JAX Mice Database - Immunological Defects

Search Criteria: Research Area is "Hematological Research: Immunological Defects"

New Strains Awaiting Transfer from the Donor
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JAX^® Mice Strains

Stock Number	Strain Name Strain Description	Standard Supply
002216	B6.129S7-Rag1^tm1Mom/J	Level 2
	Mice homozygous for the Rag1^tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency (Prkdc^scid/Prkdc^scid) (Prkdc^scid mice produce some B cells and IgM). They have no CD3⁺ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice contains 15 to 130 times fewer cells than heterozygous or wildtype siblings. The thymocytes are CD8^-CD4^- and most are IL2 receptor-positive. Neither the spleen nor the bone marrow contain any IgM or IgD staining cells, indicating an absence of mature B cells. These and other data suggest that B cell and T cell development has been arrested at an early stage. Macroscopically, the mutants are indistinguishable from heterozygotes or normal wildtype siblings.
002251	B6.129P2-Il10^tm1Cgn/J	Level 3
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full phenotype on the strain data sheet
002650	B6.129S2-Il6^tm1Kopf/J	Level 3
	Mice homozygous for the targeted mutation are viable and fertile. No gene product (mRNA) is detected by RT-PCR analysis of lipopolysaccharide (LPS) challenged macrophages. Bioassay and enzyme-linked immunosorbent assay (ELISA) analysis of serum from LPS-challenged homozygotes reveals no detectable protein activity. These interleukin 6 (IL6) mutant mice show defects in responses to various viruses and in inflammatory responses to tissue damage or infection. Of note, IL6-mutant mice may be available on different genetic backgrounds including mixed B6;129S2 (Stock No. 002254), C57BL/6J (Stock No. 002650), and BALB/cByJ.
007799	NOD.Cg-Rag1^tm1Mom Il2rg^tm1Wjl/SzJ	Level 3
	Females homozygous for both the Rag1^null and IL2rγ^null mutations (and males homozygous for Rag1^null and hemizygous for the X-linked IL2rγ^null mutation) are viable and fertile. When compared to NOD-scid IL2rg^null (Stock No. 005557), these NOD-Rag1^null IL2rγ^null mice tolerate much higher levels of irradiation conditioning. Additionally, NOD-Rag1^null IL2rγ^null mice support higher levels of both human cord blood stem cell engraftment following irradiation-conditioning (leading to multi-lineage hematopoietic cell populations and a complete repertoire of human immune cells, including human T cells) and human peripheral blood mononuclear cells engraftment in unconditioned adult mice with respect to NOD-Rag1^null (Stock No. For more information please see the full phenotype on the strain data sheet
002118	B6.129P2-Tcrb^tm1Mom/J	Level 4
	Mice homozygous for the Tcrb^tm1Mom targeted mutation are viable and fertile. Mice are deficient in alpha beta T-cell receptor. The total number of cells in the thymus is ~8% that of wildtype; CD4⁺CD8⁺ cells ~6% of wildtype. The proportion of CD4^-CD8^- (IL2 receptor positive) cells increases to about 50% of the total cell number. Alpha beta thymocyte differentiation is blocked at an earlier stage than the Tcra^tm1Mom strain. There is normal differentiation of gamma delta thymocytes. Mice may develop inflammatory bowel disease beginning at ~4-6 months of age.
002365	B6.129S-Cybb^tm1Din/J	Level 4
	Chronic granulomatous disease (CGD) is a recessive disorder characterized by a defective phagocyte respiratory burst oxidase, life-threatening pyogenic infections and inflammatory granulomas. Gene targeting was used to generate mice with a null allele of the gene involved in X-linked CGD, which encodes the 91 kD subunit of the oxidase cytochrome b. Affected hemizygous male mice lack phagocyte superoxide production, manifest an increased susceptibility to infection with Staphylococcus aureus and Aspergillus fumigatus and have an altered inflammatory response in thioglycollate peritonitis. This animal model should aid in developing new treatments for CGD and in evaluating the role of phagocyte-derived oxidants in inflammation.
002116	B6.129S2-Tcra^tm1Mom/J	Level 4
	Mice homozygous mice for the Tcra^tm1Mom targeted mutation are viable and fertile. They are deficient in the alpha beta T-cell receptor. The thymus is devoid of CD4⁺CD8^- and CD4^-CD8⁺ cells. Normal numbers of CD4⁺CD8⁺ cells are retained without the IL2 receptor. There are normal numbers of CD4^-CD8^- cells. ~1% of the thymocytes express the gamma delta TCR. Mice may develop inflammatory bowel disease beginning at ~4-6 months of age.
002287	B6.129S7-Ifng^tm1Ts/J	Level 4
	Mice homozygous for the Ifng^tm1Ts targeted mutation are viable and fertile. Homozygotes appear normal in a "clean" environment but display reduced macrophage function in response to pathogens. Specifically, macrophages show impaired production of antimicrobial products and reduced expression of MHC II antigens. There is also uncontrollable proliferation of splenocytes from homozygotes in response to mitogens and alloantigens and a reduced resting natural killer cell activity.
003008	B6;129S-Tnf^tm1Gkl/J	Level 4
	Mice homozygous for the Tnf^tm1Gkl targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does ..... For more information please see the full phenotype on the strain data sheet
002286	C.129S7(B6)-Ifng^tm1Ts/J	Level 4
	Mice homozygous for the Ifng^tm1Ts targeted mutation are viable and fertile. Homozygotes appear normal in a "clean" environment but display reduced macrophage function in response to pathogens. Specifically, macrophages show impaired production of antimicrobial products and reduced expression of MHC II antigens. There is also uncontrollable proliferation of splenocytes from homozygotes in response to mitogens and alloantigens and a reduced resting natural killer cell activity.
003145	C.129S7(B6)-Rag1^tm1Mom/J	Level 4
	Mice homozygous for the Rag1^tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency (Prkdc^scid/Prkdc^scid) (Prkdc^scid mice produce some B cells and IgM). They have no CD3⁺ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice contains 15 to 130 times fewer cells than heterozygous or wildtype siblings. The thymocytes are CD8^-CD4^- and most are IL-2 receptor positive. Neither the spleen nor bone marrow contain any IgM or IgD staining cells, indicating an absence of mature B cells. These and other data suggest that B cell and T cell development has been arrested at an early stage. Macroscopically, the mutants are indistinguishable from heterozygotes or wildtype siblings.
004326	C3Bir.129P2(B6)-Il10^tm1Cgn/Lt	Level 4
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full phenotype on the strain data sheet
000684	NZB/BlNJ	Level 4
	NZB/BlNJ mice display a number of autoimmune abnormalities including hemolytic anemia, elevated levels of immunoglobulin, anti-DNA antibodies, anti-thymocyte antibodies, and circulating immune complexes causing glomerulonephritis. F1 hybrids of NZB/BlNJ and NZW/LacJ (NZBWF1/J, Stock No. 100008) are widely used as a model for autoimmune disease resembling human systemic lupus erythematosus. NZB/BlNJ mice, fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat), fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 000668, C57BR/cdJ, Stock No. 000667, and SM/J, Stock No. 000687).
001058	NZW/LacJ	Level 4
	NZW mice have a normal lifespan but do develop anti-DNA antibodies, high serum levels of retroviral gp70 antigen, and nephritis later in life. F1 hybrids of NZB/BlNJ and NZW/LacJ (Stock No. 100008) are widely used as a model for autoimmune disease resembling human systemic lupus erythematosus.
004368	129(B6)-Il10^tm1Cgn/J	Repository- Live
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full phenotype on the strain data sheet
002250	B10.129P2(B6)-Il10^tm1Cgn/J	Repository- Live
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full phenotype on the strain data sheet
007750	B6(C)-Mir150^tm1Rsky/J	Repository- Live
	Mice homozygous for this targeted allele (miR150^-/- or MiR-150^-/-) are viable and fertile with normal development of T cells, follicular B cells, and MZ B cells. No miR-150 is expressed in spleen, mesenteric lymph node, and thymus of homozygotes. Homozygous mice exhibit B cell expansion (CD19⁺B220loCD5⁺CD43⁺CD23^-; B1a subset) in spleen and peritoneal cavity (with reciprocal reduction in B2 cells) and enhanced humoral immune response (increased serum immunoglobulins of various classes both at steady-state and following T cell-dependent antigen exposure). Homozygous miR-150 deficiency also leads to enhanced induction of the miR-150 target protein c-Myb in activated B and T cells, but no reported change in expression of the miR-150 target genes Foxp1 or ZFP91 in resting or activated B cells. These miR150^-/- mice may be useful in mircoRNA biology, specifically to study the role of miR-150 and its target genes (inc ..... For more information please see the full phenotype on the strain data sheet
004742	B6(Cg)-Ncf1^m1J/J	Repository- Live
	Peritoneal neutrophils and macrophages, bone marrow cells and neutrophils isolated from bone marrow of mice homozygous for Ncf1^m1J fail to produce superoxide upon stimulation in vitro with N-formyl-methionyl-leucyl-phenylalanine (fMLP) or phorbol 12-myristate 13-acetate (PMA), as determined by kinetic spectrophotometric analysis of cytochrome c reduction. Western blot analysis detected no full-length NCF1/p47^phox protein in cells from these mice; a faint band of slightly smaller molecular size than the wild type NCF1 protein was observed on probing with antibodies to NCF1. To exclude the possibility that the NCF1 protein is produced in cells of mutant mice but is degraded rapidly by endogenous proteases, bone marrow cells were isolated and samples prepared for western blot analysis in the presence of diisopropyl fluorophosphate (DFP); no difference was observed upon analysis of freshly prepared cell lysates made with and without DFP, indicatin ..... For more information please see the full phenotype on the strain data sheet
008449	B6(Cg)-Rag2^tm1.1Cgn/J	Repository- Live
	These RAG-2^del mutant mice harbor a pan deletion of exon 3 of the targeted locus. Homozygotes (RAG-2^del/del) are viable and fertile, with pan deletion of the entire RAG-2 protein coding region. Homozygous mice may be expected to have the same knockout phenotype as other RAG-2 null mutants or similarly created RAG-2 exon 3 pan-deleted mutants; with hematopoietic and immune system defects including arrested B cell and T cell development at the pro-B and the pro-T cell stages, respectively. These RAG-2^del mice may be useful in studying the role of RAG-2 in B cell and T cell development (including cancer and toxicology research as a xenograft/transplant host), T and B cell receptor (V(D)J) recombination, hematopoiesis, hematology, immunology, and inflammation research. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was ..... For more information please see the full phenotype on the strain data sheet
005085	B6.129(Cg)-Cd44^tm1Hbg/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected. Although lymphocyte development appears unremarkable, irregularities are observed in lymphocyte trafficking. Tail-injected lymphocytes derived from null animals exhibit an impaired ability to traffic to peripheral lymph nodes, and to a much greater degree, the thymus. Transcription and translation of the targeted allele subsequently lead to the synthesis of the lacZ protein under control of the 5' regulatory elements of the endogenous locus in all cells and tissues normally expressing one or several of the CD44 isoforms. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary f ..... For more information please see the full phenotype on the strain data sheet
016163	B6.129-Gfi1^{tm3(Gfib1)Tmo}/J	Repository- Live
	These mutant mice express mouse Gfi1b (growth factor independent 1B) from the endogenous Gfi1 locus. Mice that are homozygous for the targeted mutation are viable, fertile and normal in size. Higher expression levels of Gfi1b transcript is detected in inner ears as measured by RT-PCR analysis. The Gfi1b knock-in did not completely rescue the Gfi1 knock out phenotype (see STOCK No. 016161). Homozygotes have slightly fewer granulocytes in bone marrow, a small accumulation in bone marrow of immature myeloid cells and monocytes, and fewer mature circulating granulocytes when compared to wildtype controls. At 3 to 3.5 months in age, homozygotes are deaf, do not display a Preyer reflex, abnormal auditory brainstem response (over 100 dB at 8 kHz and over 90 dB at 16 and 32 kHz), and exhibit head bobbing and abnormal reaching response. In neonatal mutants, the cochlear inner hair cells are morphol ..... For more information please see the full phenotype on the strain data sheet
017700	B6.129-Rag1^tm1Mom Fcgrt^tm1Dcr/DcrJ	Repository- Live
	Rag1-/- mFcRn-/- mice are immunodeficient. This strain serves as a control strain for 016919
006621	B6.129P2(C)-Ccr7^tm1Rfor/J	Repository- Live
	Homozygous mice are viable and fertile and show delayed primary B or T cell immune responses. Lymph nodes from homozygous mice are devoid of naive T cells and dendritic cells (DCs), but the T cell populations in the blood, the red pulp of the spleen, and in the bone marrow are greatly expanded. Secondary lymph organs exhibit morphological abnormalities, and adoptive transfer experiments demonstrate impaired B- and T-cell migration. In a model of acute allogeneic tumor rejection, homozygous mice fail to reject subcutaneously injected MHC class I mismatched tumor cells, and cytotoxic activity of allospecific T cells is severely compromised. These mutant mice (along with CXCR5-deficient mice - Stock No. 006659) - may be useful in immunological studies of chemokine receptors, including T- and B-cell function in primary and adaptive immune responses, entry of lymphocytes and dendritic cells into secondary lymphoid organs (and their hom ..... For more information please see the full phenotype on the strain data sheet
002252	B6.129P2-Il2^tm1Hor/J	Repository- Live
	Homozygous mutant mice show no apparent deficit in thymocyte differentiation or selection, types and numbers of T cells from spleens and lymph nodes are comparable to those of wild-type. They do have an impaired response to polyclonal T cell activators in the absence of additional IL2, deficits in their helper function and a reduction in natural killer cell activity. There is significant pre-weaning and post-weaning loss of homozygotes on the C3H/HeJCrlBR and C57BL/6J genetic backgrounds. In addition, homozygous mice develop inflammatory bowel disease between six and 15 weeks of age and reportedly die within 10-25 weeks under conventional housing conditions. Homozygotes on the C57BL/6J genetic background show an atrophied pancreas with apparently intact islets. Homozygotes on the BALB/c genetic background do not develop inflammatory bowel disease symptoms but rather die three to five weeks postnatally of a form of hemolytic anemia. For a more detailed description please refer to the ..... For more information please see the full phenotype on the strain data sheet
004781	B6.129P2-Lyz2^tm1(cre)Ifo/J	Repository- Live
	This strain expresses Cre recombinase from the endogenous Lyzs locus. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in deletion of the targeted gene in the myeloid cell lineage, including monocytes, mature macrophages, and granulocytes. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This strain represents an effective tool for generating myeloid cell-specific targeted mutants. View cre expression characterization.
008336	B6.129P2-Ptpn6^tm1Rsky/J	Repository- Live
	Mice homozygous for the Ptpn6^f allele are viable and fertile, with loxP sites flanking exon 1(II) through most of exon 9 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have this region deleted in cre-expressing tissue(s). These Ptpn6^f mice may be useful in generating conditional mutations for studying the role of Ptpn6 (Shp1) in inflammation and immunology research. For example, when bred to a strain with inducible Cre recombinase expression in liver and lymphocytes (see Stock No. 003556), this mutant mouse strain may be useful in studying the motheaten (me) phenotype; characterized by widespread inflammation and autoimmunity. When bred to a strain with a Cd19 null allele and expressing Cre recombinase during the B lymphocyte development (Stock No. 004126, Stock No. > ..... For more information please see the full phenotype on the strain data sheet
002122	B6.129P2-Tcrb^tm1Mom Tcrd^tm1Mom/J	Repository- Live
	Mice homozygous for both the Tcrb^tm1Mom and the Tcrd^tm1Mom targeted mutations express no alpha beta T-cell receptor nor any gamma delta T-cell receptor. Under certain housing conditions homozygous mutant mice develop mild inflammatory bowel disease.
002120	B6.129P2-Tcrd^tm1Mom/J	Repository- Live
	Mice homozygous for the Tcrd^tm1Mom targeted mutation are viable and fertile. Gamma delta T-cell receptor expression is deficient in all adult lymphoid and epithelial organs. There is normal development of the alpha beta T-cell lineage. Patterns of CD4⁺CD8^- and CD4^-CD8⁺ alpha beta T-cells are apparently normal. Mice do not develop inflammatory bowel disease.
016222	B6.129S(Cg)-Id2^{tm1.1(cre/ERT2)Blh}/ZhuJ	Repository- Live
	The Id2-CreERT2 knockin allele was designed to both abolish inhibitor of DNA binding 2 (Id2) gene function and express CreER^T2 fusion protein from the Id2 promoter/enhancer elements. Cre-ERT2 fusion gene activity is inducible and can be observed following tamoxifen administration. As such, when Id2-CreERT2 knockin mice are bred with mice containing loxP-flanked sequences, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Id2-expressing cells of the offspring. No mRNA or protein expression from the Id2-CreERT2 allele is observed. The donating investigator reports that homozygous mice are runted with defective lung alveolarization. Other organ systems have not been evaluated. However, Id2-CreERT2 homozygotes may be expected to exhibit the same phenotype as mice homozygous for other null mutations of this gene (including postnatal lethality and defects of the immune system, digestive tract, ..... For more information please see the full phenotype on the strain data sheet
005540	B6.129S-Tnf^tm1Gkl/J	Repository- Live
	Mice homozygous for the targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does not affect the degree of obe ..... For more information please see the full phenotype on the strain data sheet
005763	B6.129S1-Nod2^tm1Flv/J	Repository- Live
	Homozygous mice are viable and fertile with normal lymphoid and myeloid cellularity and no intestinal inflammation up to 6 months of age. Homozygotes do not express the targeted gene in spleen or intestinal crypts. Null mice, as well as antigen presenting cells derived from them, lack the protective immunity (IgG1, interleukin-6, and NF-kappaB-related responses) normally afforded by endogenous protein recognition of its ligand, bacterial muramyl dipeptide (MDP). Mice homozygous for the mutation have increased susceptibility to oral (intragastric) bacterial challenge and diminished cryptdins. This mouse may be useful in studies of Crohn's disease and other inflammatory bowel diseases, innate immunity, signal transduction, and bacterial susceptibility.
006144	B6.129S2(C)-Itgae^tm1Cmp/J	Repository- Live
	Mice that are homozygous for this targeted mutation are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. No endogenous gene expression is detected in intraepithelial lymphocytes by FACS analysis or on TGF-beta1-treated splenocytes by immunoprecipitation. Homozygous null mice exhibit reduced numbers of intestinal intraepithelial lymphocytes and lamina propria lymphocytes. These mice may be useful in studies of the immune system, including T cell function. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
005977	B6.129S2(C)-Stat6^tm1Gru/J	Repository- Live
	Homozygous mice are viable and fertile with no behavioral abnormalities. Homozygotes do not express the endogenous protein in thymus and peripheral lymphoid organs. In contrast to controls, IL-4 treated lymphocytes show no induction of MHC class II or IL-4 receptor genes and have severly impaired proliferative responses. Further, homozygous mice have a defective IgE response. While T-helper 1 (Th1) cell differentiation is unimpaired in homozygous splenocytes, Th2 cell differentiation is almost completely abrogated despite IL-4 or IL-13 incubation. Myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) is more severe in homozygous mice compared to wildtype. This mouse may be useful in studies of Th2 cell differentiation, Th2-mediated diseases, asthma, cytokine/chemokine function, signal transduction and transcription factors, and diseases of the central nervous system such as multiple sclerosis.
006659	B6.129S2(Cg)-Cxcr5^tm1Lipp/J	Repository- Live
	Homozygous (CXCR5-deficient) mice are viable and fertile. Multiple lymphoid organs lack detectable levels of targeted protein expression using flow cytometry, and RNA transcripts are also absent in spleen cells. Homozygous mutant mice exhibit a complex pattern of lymph node (LN) developmental defects (e.g. deficient in inguinal, iliac and parathymic LN, but apparently normal mesenteric LN) accompanied by impaired Peyer's patch development. In addition, CXCR5-deficient mice show a completely disorganized splenic microarchitecture, lacking segregated T- and B-cell areas within the splenic white pulp. These mutant mice (along with CCR7-deficient mice: Stock No. 006621) may be useful in immunological studies of chemokine receptors, including T- and B-cell function in primary and adaptive immune responses, entry of lymphocytes and dendritic cells into secondary lymphoid organs and their homing to T- and B-cell zones therein. In ..... For more information please see the full phenotype on the strain data sheet
013152	B6.129S2(Cg)-Fut7^tm1Jbl Fut4^tm1Jbl/J	Repository- Live
	In this strain the catalytic domains of the fucosyltransferase 4 (Fut4) gene and the fucosyltransferase 7 (Fut7) gene were replaced with neomycin resistance (neo) cassettes, abolishing gene function. Mice homozygous for both alleles are viable, fertile, and normal in size. These mice lack inflammation-dependent leukocyte recruitment; specifically neutrophils, eosinophils, monocytes, T cells and dendritic cells are unable to migrate to extravascular sites of acute and chronic inflammation. The peripheral nodes in these mice do not support normal B lymphocyte or naive T lymphocyte homing. FucTIV-null defects in leukocyte E- and P-selectin counterreceptor activity and HEV-born L-selectin ligand activity are reversed in the double null mutant mice. Neutrophils in the doubly null mice, unlike FucT-7VII null leukocytes, are virtually devoid of E- and P-selectin ligand activities. These mice also exhibit extreme leukocytosis characterized by decreased neutrophil turnover and in ..... For more information please see the full phenotype on the strain data sheet
008102	B6.129S4-Ltb4r1^tm1Adl/J	Repository- Live
	Mice homozygous for this BLTR (BLT1)-deficient allele are viable and fertile. Northern blot analysis of neutrophils, macrophages, lymph nodes, lungs, and spleens isolated from homozygous mice show absence of the normal transcript and presence of the expected larger transcript (due to the insertion of the neomycin resistance cassette in exon 2 of the targeted gene), albeit at lower levels than the wild type transcript. Homozygous disruption of this allele confers impaired leukocyte function (chemotaxis, recruitment, firm adhesion). For example, homozygotes exhibit substantially diminished recruitment of eosinophils in a model of peritonitis, effector T cells in a model of allergic pulmonary inflammation, and neutrophils in a model of rheumatoid arthritis. As the G protein-coupled receptor BLTR/BLT1 is expressed on myeloid leukocytes (including neutrophils, macrophages, eosinophils, T cell lymphomas, and effector T cells (TH1 CD4⁺ cells, TH2 CD4⁺ cells, and effecto ..... For more information please see the full phenotype on the strain data sheet
015861	B6.129S4-Pglyrp1^tm1.1Lky/J	Repository- Live
	These PGRP-S mice contain a targeting vector designed to insert an enhanced yellow fluorescent protein (EYFP) immediately downstream from the initiation sequence of the peptidoglycan recognition protein, 1 (Pglyrp1) gene, abolishing gene expression. Homozygous mice are viable, fertile, normal in size and do not display any gross physical abnormalities. PGRP-S, belongs to a family of innate immune recognition molecules, and recognizes peptidoglycan components of bacterial cell walls. Expressed mainly in neutrophil tertiary granules, PGRP-S is secreted and multimerizes in the serum. These PGRP-S-/- mice have normal inflammatory responses and production of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6). PGRP-S knockout mice have increased susceptibility to intraperitoneal infection with gram-positive bacteria of low pathogenicity, but not with more pathogenic gram-positive or gram-negative bacteria. Neutrophils from PGRP-S-/- mice have normal phagocytic upta ..... For more information please see the full phenotype on the strain data sheet
015860	B6.129S4-Pglyrp2^tm1Lky/J	Repository- Live
	These PGRP-L mice contain a targeting vector designed to insert an enhanced green fluorescent protein (EGFP) immediately downstream from the initiation sequence of the peptidoglycan recognition protein, 2 (Pglyrp2) gene, abolishing gene expression. Homozygous mice are viable, fertile, normal in size and do not display any gross physical abnormalities. PGRP-L, the longest member of a family of innate immune recognition molecules, recognize peptidoglycan components of bacterial cell walls. Expressed mainly in liver, PGRP-L is secreted and multimerizes in the serum. Peritoneal macrophages from these PGRP-L-deficient mice showed a decrease in interleukin 6 (IL6) and tumor necrosis factor alpha (TNFα) production when stimulated with E. coli or lipopolysaccharide (LPS), but comparable amounts when stimulated with S. aureus, C. albicans, gram-positive or -negative peptidoglycans, suggesting a redundant pathway is involved. These mice may be useful for visualizing PGRP-L expre ..... For more information please see the full phenotype on the strain data sheet
010672	B6.129S4-Tnfrsf11b^tm1Eac/J	Repository- Live
	Mice homozygous for this osteoprotegerin (OPG)-mutant allele are viable and fertile. While a smaller transcript is made from the disrupted allele, the spliced product is predicted to be out of frame and result in a nonfunctional protein. OPG-deficient mice exhibit dysregulation of osteoclast production leading to drastic changes in the bone architecture; homozygotes develop severe osteoporosis, gross deformations in bone structure, decreased bone density, and altered long bones physical dimension. Hematopoietic, B lymphocyte, and dendritic cell functions are also dysregulated. It has been the experience of The Jackson Laboratory that animals homozygous for the Tnfrsf11b^tm1Eac exhibit significant (~50%) pre-wean mortality. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype ..... For more information please see the full phenotype on the strain data sheet
004088	B6.Cg-Foxp3^sf/J	Repository- Live
	Scurfy mice develop an X-linked lymphoproliferative disease resulting from defective T cell tolerance. Phenotypes associated with these mice include runting, scaly, crusty skin on the eyelids, ears and tails, dermal thickening, squinted eyes, cachexia, reddening and swelling of the genital papilla, and small testicles that are retained in the abdominal cavity. This disorder, which parallels X-linked autoimmunity-allergic disregulation syndrome (XLAAD) in humans, results in Coombs' test-positive anemia, hypergammaglobulinemia, a small, thin thymus, and lymphohistiocytic proliferation in the skin and lymphoid organs, with splenomegaly, lymphadenomegaly, and hepatomegaly. Foxp3^sf/Y males generally die by 16-25 days of age. Transgenic expression of Foxp3 prevents scurfy disease in Foxp3^sf/Y mice. Neonatal thymectomy of scurfy males ameliorates disease and increases lifespan; athymic nude (Foxn1^nu/Foxn1^nu) ..... For more information please see the full phenotype on the strain data sheet
006908	B6.Cg-Ikbke^tm1Tman/J	Repository- Live
	Homozygous IKKepsilon mutant mice are viable and fertile. Homozygous deletion results in a complete loss of the endogenous kinase function in lung, spleen, and embryonic fibroblasts. These mice have increased susceptibility to viral infection due to defective inteferon (IFN) signaling. These IKKepsilon mutant mice may be useful in immunological studies involving IFN signaling and host responses to infection.
012566	B6.Cg-Mapk11^tm1Jda Mapk14^tm1Jda/J	Repository- Live
	Mice homozygous for both polymorphic alleles (p38αβ^Y323F) are viable, fertile and of normal size and weight. Each mutation introduces a tyrosine to phenylalanine at codon 323 (Y323F) within exon 11 of their respective locus; this prevents phosphorylation of residue 323 for each protein. While each polymorphism should have no direct affect on canonical MAPK cascade-induced p38 activation, the T cell receptor (TCR)-mediated alternative activation pathway of p38 activation is abolished in homozygous p38αβ^Y323F mice. Accordingly, activation-induced p38 phosphorylation in p38αβ^Y323F T cells is reduced relative to the respective contribution of each isoform to total T cell p38 activity (p38β^Y323F > p38α^Y323F > p38αβ^Y323F). This failure to activate both the p38α and p38β isoforms in T cells via TCR engagement results in impaired T cell proliferation compare ..... For more information please see the full phenotype on the strain data sheet
007745	B6.Cg-Mir155^tm1.1Rsky/J	Repository- Live
	Mice homozygous for this loss-of-function/reporter allele (bic/mir-155-/-) are viable and fertile. The lacZ reporter allows the detection of bic promoter transcriptional activity using fluorescence activated cell sorting (FACS). In homozygotes, miR-155 expression is undetectable in activated splenic B cells. In heterozygotes, approximately 60% of germinal center (GC) B cells express the lacZ reporter whereas the vast majority of the non-GC B cells do not. Homozygous mice exhibit a reduced fraction of GC B cells in the gut-associated lymphoid tissue (GALT; including Peyer's patches (PPs) and mesenteric lymph nodes (mLNs)). In addition, bic/miR-155-/- B cells exhibit deficient tumor necrosis factor (TNF) and lymphotoxin-α (LT-α) cytokine production. Homozygous mice show impaired T cell-dependent antibody responses, and their T cells show a TH2 cytokine bias (an increased percentage of interleukin-4 (IL-4) producing cells and a decreased percentage of interferon-γ (IFN-& ..... For more information please see the full phenotype on the strain data sheet
008684	B6.Cg-Rag1^tm1Mom Tyrp1^B-w Tg(Tcra,Tcrb)9Rest/J	Repository- Live
	These mice are hemizygous for the TRP-1 transgene Tg(Tcra,Tcrb)9Rest, homozygous for the targeted mutation Rag1^tm1Mom and homozygous for the white based brown radiation induced mutation of tyrosinase-related protein 1, Tyrp1^B-w. These mutant mice express a MHC class II-restricted TCR recognizing the endogenous melanocyte differentiation antigen minimal TRP-1 (tyrosinase-related protein 1) epitope corresponding to amino acids 113 to 127. The transgene is located on the Y chromosome in founder line 9. On a RAG-deficient background, these mice are also homozygous for the Tyrp1^B-w mutation and do not produce endogenous tyrosinase-related protein 1. This strain is a source for melanocyte reactive CD4⁺ cells from antigen-negative animals and may be useful in studies of cancer immunology and therapeutics.
016919	B6.Cg-Rag1^tm1Mom Fcgrt^tm1Dcr Tg(CAG-FCGRT)276Dcr/DcrJ	Repository- Live
	These mFcRn-/- hFcRn (276) Tg mice are homozygous for the knockout mutation of the FcRn α-chain (Fcgrt^tm1Dcr) and express a human FcRn α-chain (FCGRT) transgene. By itself, the homozygous Fcgrt KO allele mice are functionally IgG deficient. They fail to transport IgG across the neonatal gut and degrade IgG at an accelerated rate. They also exhibit a plasma albumin deficiency. While the hFcRn (276) transgene corrects the relative albumin deficiency caused by the FcRn α-chain knockout, expression of the hFcRn (276) transgene is unable to bind and protect murine IgG from degradation in FcRn α-chain null mice. Importantly, hFcRn (276) transgene expression is protective against the rapid decay rate of administered human IgG. Human antibodies engineered to have enhanced binding to FCGRT (Hu4D5-IgG1, directed against human epidermal growth factor receptor 2) exhibit a significant increase in their serum half-life (2-2.5 fold) in ..... For more information please see the full phenotype on the strain data sheet
004369	B6.Cg-Rag1^tm1Mom Ins2^Akita/J	Repository- Live
	Mice homozygous for the Rag1 targeted mutation and heterozygous for the Akita spontaneous display the diabetes phenotype in the absence of B and T cells and unlike single Akita mice, double mutants do not reject allografts. Mice heterozygous for only the Akita spontaneous mutation are viable and fertile. (Homozygotes typically die by 12 weeks of age from extreme hyperglycemia.) Symptoms in heterozygous mutant mice include hyperglycemia, hypoinsulinemia, polydipsia, and polyuria, beginning at approximately 3-4 weeks of age. The diabetic phenotype is more severe and progressive in heterozygous males than in females. Obesity and insulitis do not accompany diabetes. This double mutant strain is ideally suited for use in allogeneic or xenogeneic islet or stem cell transplantation protocols because the mice are severely immunocompromised and spontaneously develop diabetes at a young age.
016911	B6.Cg-Tg(Gata1-CR1)1Rwf/J	Repository- Live
	These transgenic mice express the human complement component (3b/4b) receptor 1 (Knops blood group), CR1, under the control of the mouse Gata1, GATA binding protein 1, promoter. Transgene expression is detected on erythrocytes by flow cytometry. Unlike erythrocytes from wildtype controls, erythrocytes from transgenic mice will adhere beads coated with human or mouse serum complement. Transgenic erythrocytes exhibit increased adherence of pneumococci and type 5 adenovirus as well as increased Plasmodium falciparum merozoite invasion when compared to wildtype controls. The donating investigator reports that this transgene is locatd on the X chromosomse. Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities.
012603	B6;129-Tgfbr2^tm1Karl/J	Repository- Live
	These TβRII floxed mutant mice possess loxP sites flanking exon 4 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 4 deleted in cre-expressing tissues. This strain may be useful for studying the cellular and mechanical role of TGF-β in regulating development, hematopoiesis, wound healing, and immune function. For example, when crossed to a strain expressing Cre recombinase in the neural tube, midbrain and dorsal spinal cord (see Stock No. 007807), this mutant mouse strain may be useful in studies of DiGeorge syndrome. For example, when crossed to a strain expressing interferon inducible Cre recombinase (see Stock No. > ..... For more information please see the full phenotype on the strain data sheet
002254	B6;129S2-Il6^tm1Kopf/J	Repository- Live
	Mice homozygous for the targeted mutation are viable and fertile. No gene product (mRNA) is detected by RT-PCR analysis of lipopolysaccharide (LPS) challenged macrophages. Bioassay and enzyme-linked immunosorbent assay (ELISA) analysis of serum from LPS-challenged homozygotes reveals no detectable protein activity. These interleukin 6 (IL6) mutant mice show defects in responses to various viruses and in inflammatory responses to tissue damage or infection. Of note, IL6-mutant mice may be available on different genetic backgrounds including mixed B6;129S2 (Stock No. 002254), C57BL/6J (Stock No. 002650), and BALB/cByJ (Stock No. 001026).
002096	B6;129S7-Rag1^tm1Mom/J	Repository- Live
	Mice homozygous for the Rag1^tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency (Prkdc^scid/Prkdc^scid) (Prkdc^scid mice produce some B cells and IgM). They have no CD3⁺ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice contains 15 to 130 times fewer cells than heterozygous or wildtype siblings. The thymocytes are CD8^-CD4^- and most are IL2 receptor positive. Neither the spleen nor bone marrow contain any IgM or IgD staining cells, indicating an absence of mature B cells. These and other data suggest that B cell and T cell development has been arrested at an early stage. Macroscopically, the mutants are indistinguishable from heterozygotes or normal wildtype siblings.
003723	B6;129X1-Il15ra^tm1Ama/J	Repository- Live
	Il15ra mediates the high-affinity binding of Il15, a pleiotropic cytokine implicated in the development of innate immune cells. Mice that are homozygous null for Il15ra are viable and fertile. They are lymphopenic as result of decreased proliferation and homing of lymphocytes to peripheral lymph nodes. As a result, marked hypocellularity of lymph nodes is observed. Deficiencies are seen in levels of natural killer cells, natural killer T cells, CD8⁺ T lymphocytes, TCR delta/gamma intraepithelial lymphocytes and memory phenotype CD8⁺ T cells. Loss of IL15RA expression has also been shown to induce a functional oxidative shift in fast muscles, substantially increasing fatigue resistance and exercises capacity. Knockout mice run greater distances and have greater ambulatory activity than control animals.
012457	B6N.129-Ptch1^tm1Hahn/J	Repository- Live
	These Ptch^flox mutant mice possess loxP sites flanking exons 8-9 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 8-9 deleted in the cre-expressing tissue. The donating investigator reports that the frt-flanked neo cassette is still present downstream of the floxed exon that the presence of neo does not convey any abnormalities. This strain may be useful for studying Hedgehog/Patched signaling, cell-fate determination during embryogenesis, cell growth and differentiation, and development of T- and B-lymphoid lineages, hematopoietic stem cell diversification.
012866	B6N.DDD-plt/NknoJ	Repository- Live
	Homozygous C57BL/6-plt mice are viable and fertile, harboring the spontaneous plt (or "paucity of lymph node T cells") deletion of both the Ccl19 and Ccl21a loci on chromosome 4. Lack of expression of these two CCR7 ligands in the secondary lymphoid organs results in abnormal leukocyte migration and impaired immune response. Specifically, homozygous mice have disrupted trafficking/homing of T cells and dendritic cells to lymphoid tissues. No reported abnormalities in B cell distribution/cellularity are reported for homozygous mice. Transient migration of antigen-stimulated B cells in lymphoid organs (which facilitates B cell/helper T cell interactions) is also impaired in homozygous mice. Homozygous mice exhibit mature single-positive thymocyte arrest in the thymic cortex that results in defective formation of the medullary region of the thymus. Thymic export of T cells in these mice is compromised during the neonatal period but not in adulthood. While C ..... For more information please see the full phenotype on the strain data sheet
004333	C.129P2(B6)-Il10^tm1Cgn/J	Repository- Live
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full phenotype on the strain data sheet
005712	C.129S4-C3ar1^tm1Cge/J	Repository- Live
	Mice homozygous for the targeted mutation are viable, fertile, normal in size, and do not display any behavioral abnormalities when maintained under barrier conditions. No transcripts from the targeted gene are detected in bone marrow. Homozygous mice have normal T and B cell development but elevated IgG1 and decreased IgG2a, IgG3, and IgA in serum. In standard models of airway hyperresponsiveness (intraperitoneal (i.p.) sensitization followed by aerosol challenge), mutant mice are protected from allergic airway disease. Following epicutaneous, but not i.p., sensitization, homozygotes have significantly greater serum IgG1, dermal eosinophilia, and splenocyte Th2 cytokine secretion. Antigen presenting cells from null mice induce stronger Th2 responses. This mutant may be suitable for use in studies related to asthma, allergic skin disease, T helper cell polarization/B cell isotype switching, and other Th2- and innate-immunity studies.
005440	C.129S4-Ccr3^tm1Cge/J	Repository- Live
	Mice homozygous for this CCR3 (chemokine (C-C motif) receptor 3) targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by RNA protection assay analysis of thymus, spleen and lung tissues. Mice homozygous for the mutation have impaired trafficking of eosinophils. A 7-fold decrease in the number of eosinophils in the small intestine and a 6-fold increase in the spleen is observed. Aerosol allergen challenge does not cause the expected infiltration of eosinophils to the lung tissue and airway lumens (50-70% reduction), although abundant eosinophils are found in the airway blood vessels. Concurrent increases in eosinophils in the spleen and intraepithelial mast cells in the spleen occur after allergen challenge. Homozygotes exhibit increased bronchoconstriction with allergen-induced airway hyperresponsiveness. There is no increase in eosinophils or eosinophil product major basic protein (M ..... For more information please see the full phenotype on the strain data sheet
008309	C57BL/6-Rag2^tm1Cgn/J	Repository- Live
	Mice homozygous for the RAG-2^fl allele are viable and fertile, with loxP sites flanking exon 3 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have this region (coding for the entire RAG-2 protein) deleted in the cre-expressing tissue(s). These RAG-2^fl mice may be useful in generating conditional mutations for studying the role of RAG-2 in B and T cell development (including cancer and toxicology research as a xenograft/transplant host), T and B cell receptor (V(D)J) recombination, hematopoiesis, hematology, immunology, and inflammation research. For example, when bred to a strain with inducible Cre recombinase expression in liver and lymphocytes (see Stock No. 003556), this mutant mouse strain may be useful in studies of B and T cell development.
014644	C57BL/6-Tg(Cd4-Zbtb16)1797Aben/J	Repository- Live
	CD4-PLZF transgenic mice contain CD4 promoter/enhancer elements driving expression of the zinc finger and BTB domain containing 16 (Zbtb16 or PLZF) cDNA from purified natural killer T (NKT cells). Hemizygous mice are viable and fertile. PLZF is a transcriptional regulator that is expressed in NKT cells and is required for their maturation into effector-type lymphocytes. Transgenic expression of PLZF using the CD4 promoter induces conventional CD4 T cells to acquire effector characteristics. While CD4 T cells are present at normal levels in the thymus, spleen, liver, and lungs of the CD4-PLZF mouse, they are nearly absent in the blood and lymph nodes. Greater than 98% of mature CD4 T cells display a CD44^hi/CD62L^lo effector phenotype. An increased percentage of CD4 T cells produce both interleukin-4 (IL-4) and interferon (IFN) γ upon TCR stimulation. These mice may be useful for studying the function of PLZ ..... For more information please see the full phenotype on the strain data sheet
016617	C57BL/6-Tg(Nr4a1-EGFP/cre)820Khog/J	Repository- Live
	Mice hemizygous for the Nur77-GFPCre BAC transgene (Nur77^GFP BAC transgenic mice) are viable and fertile with normal lymphoid and myeloid development. Nur77-GFPCre BAC transgenic mice express an enhanced green fluorescent protein/codon-optimized "humanized" Cre recombinase fusion protein (eGFP-hCre) under control of the Nr4a1 (Nur77) promoter/enhancer regions within the BAC transgene. Nur77-GFPCre BAC transgenic mice from founder line B6-820 exhibit GFP expression patterns consistent with endogenous Nur77. Specifically, GFP is highly expressed in a subset of myeloid lineage cells of the spleen (but not lymph node), while low levels of GFP are observed in T and B lymphocytes. GFP is up-regulated by antigen receptor stimulation in Nur77-GFPCre BAC transgenic mice, but unlike the CD69 marker of T cell activation, GFP is not induced by inflammatory stimuli. Furthermore, the level of GFP expressed during acute activation reflects the strength of T cell receptor (TCR) stim ..... For more information please see the full phenotype on the strain data sheet
000629	C57BL/6J-Lyst^bg-J/J	Repository- Live
	Mice homozygous for the beige-J spontaneous mutation (Lyst^bg-J) are identical to the original beige mutation (Lyst^bg). The phenotype closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syn ..... For more information please see the full phenotype on the strain data sheet
014594	C;129S4-Rag2^tm1.1Flv Thpo^{tm1.1(TPO)Flv} Il2rg^tm1.1Flv/J	Repository- Live
	This compound mutant strain carries deletions in the Rag2 and X-linked Il2rg genes in addition to a targeted replacement of mouse Thpo (thrombopoietin) coding sequences with those of the human gene. Triple homozygotes (hemizygous/homozygous for the Il2rg mutation) lack T, B and NK cells and express human THPO in the same tissues as mouse Thpo, although at a lower concentration. Homozygous humanization of THPO leads to significantly increased levels of human cell engraftment in the bone marrow of hosts, and multilineage differentiation of hematopoietic cells is improved. An increased ratio of myelomonocyte versus lymphoid lineages is also seen. The self-renewal capacity of engrafted human stem and progenitor cells is improved. The creation of this strain was funded by the Bill and Melinda Gates Foundation.
007082	CByJ.129S(B6)-Tnf^tm1Gkl/J	Repository- Live
	Mice homozygous for the Tnf^tm1Gkl targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does ..... For more information please see the full phenotype on the strain data sheet
007078	CByJ.129S2(B6)-Il6^tm1Kopf/J	Repository- Live
	Mice homozygous for the targeted mutation are viable and fertile. No gene product (mRNA) is detected by RT-PCR analysis of lipopolysaccharide (LPS) challenged macrophages. Bioassay and enzyme-linked immunosorbent assay (ELISA) analysis of serum from LPS-challenged homozygotes reveals no detectable protein activity. These interleukin 6 (IL6) mutant mice show defects in responses to various viruses and in inflammatory responses to tissue damage or infection. Of note, IL6-mutant mice are available on different genetic backgrounds including mixed B6;129S2 (Stock No. 002254), C57BL/6J (Stock No. 002650), and BALB/cByJ (Stock No. 007078). In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phe ..... For more information please see the full phenotype on the strain data sheet
003729	NOD.129S7(B6)-Rag1^tm1Mom/J	Repository- Live
	Mice homozygous for the Rag1^tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency. (Prkdc^scid/Prkdc^scid) mice produce some B cells and IgM. NOD.129S7(B6)-Rag1^tm1Mom/J mice have no CD3⁺ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice is severely involuted. The thymocytes are CD8^-CD4^- and most are IL2 receptor positive. Neither the spleen nor bone marrow contain any IgM or IgD staining cells, indicating an absence of mature B cells. These and other data suggest that both B cell and T cell development have been arrested at an early stage. Macroscopically, the mutants are indistinguishable from heterozygotes or normal wildtype siblings. Notable differences between this strain and the NOD.CB17-Prkdc^scid/J strain (Stock No. 001303) include a longer life s ..... For more information please see the full phenotype on the strain data sheet
010606	NOD.Cg-Ncf1^m1J/MxJ	Repository- Live
	On the C57BL/6 background, Peritoneal neutrophils and macrophages, bone marrow cells and neutrophils isolated from bone marrow of mice homozygous for Ncf1^m1J fail to produce superoxide upon stimulation in vitro with N-formyl-methionyl-leucyl-phenylalanine (fMLP) or phorbol 12-myristate 13-acetate (PMA), as determined by kinetic spectrophotometric analysis of cytochrome c reduction. Western blot analysis detected no full-length NCF1/p47^phox protein in cells from these mice. Analysis for other NADPH oxidases involved in neutrophil superoxide production revealed that NCF2/p67^phox was present at wild type levels and CYBB/gp91^phox and CYBA/p22^phox were expressed at higher than wild type levels. Other neutrophil products were assayed and found not to differ in bone marrow cells of C57BL/6J vs. mutant mice; (Huang et al. 2000). NOD.Ncf1 deficient mice lack functional NADPH oxidase enzymes and a ..... For more information please see the full phenotype on the strain data sheet
008659	NOD.Cg-Rag1^tm1Mom Ins2^Akita Prf1^tm1Sdz/SzJ	Repository- Live
	Like NOD.Cg-Rag1^tm1Mom Prf1^tm1Sdz/J (004848), this strain lacks mature T and B cells. NK cells, although present, lack cytotoxic activity. Both sexes develop spontaneous hyperglycemia as early as three weeks of age, however, the phenotype is predominantly exhibited by males. Pancreatic islets have reduced insulin staining and exhibit an altered morphology with age. Human islet transplantation at doses of 4000 IEQ is successful in returning hyperglycemic males to a euglycemic state. This strain may useful in studies of human islet and beta stem and progenitor cell function.
004848	NOD.Cg-Rag1^tm1Mom Prf1^tm1Sdz/SzJ	Repository- Live
	Mice that are homozygous for both targeted mutations are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities when housed under specific pathogen free conditions. These double homozygote mutant mice have no mature T or B lymphocytes, no detectable NK cell cytotoxic activity, and lack serum immunoglobulin. The number of nucleated spleen cells is significantly reduced in double mutant mice, when compared to the single homozygote, NOD.129S7(B6)-Rag1^tm1Mom/J (Stock No. 003729). Although an increased number of DX5⁺CD122⁺ NK cells are found in the spleens of double mutants, these NK cells have impaired cytotoxic activity. The disruption of Prf1 ablates NK cell cytotoxic activity resulting in increased engraftment levels over that observed with Stock No. 003729. All mutant mice develop thymic lymphomas. This double mutant mouse strain may be useful in studies involving engraftment of human hematolympho ..... For more information please see the full phenotype on the strain data sheet
014568	NOD.Cg-Rag1^tm1Mom Ins2^Akita Il2rg^tm1Wjl/SzJ	Repository- Live
	NRG-Akita mice, which are homozygous for the Rag1^tm1Mom and the Il2rg^tm1Wjl alleles (males are hemizygous for the X-linked Il2rg^tm1Wjl allele) and heterozygous for the Ins2^Akita allele, develop spontaneous hyperglycermia. No mature T, B or NK cells are detected in flow cytometric analysis of splenocytes from NRG-Akita mutant mice. Granulocyte and macrophage populations are similar to those seen in NRG mice (Stock No. 7799). NRG-Akita mice develop hyperglycemia between 3 and 5 weeks of age. Histological examination at 3 weeks of age reveals normal pancreas morphology, and routine insulin and glucagon staining. By approximately 32 weeks of age, NRG-Akita mice display disorganized, condensed pancreatic islet architecture, with loss of insulin-positive cells. Euglycemia is restored by subrenal transplantation of mouse or human islets or intrapancreatic transplantation of dissociated mouse islet cells. NRG-Akita ..... For more information please see the full phenotype on the strain data sheet
009377	NOD.Cg-Rag1^tm1Mom Tg(TcraBDC12-4.1)10Jos Tg(TcrbBDC12-4.1)82Gse/J	Repository- Live
	This double transgenic, targeted mutation strain carries a rearranged Tcr beta gene and a Tcr alpha gene from the pathogenic anti-insulin CD4⁺ T-cell clone BDC12-4.1 and NOD.Rag1^tm1Mom targeted mutation (Stock No. 003729). Triple mutant mice are viable and fertile. When the congenic NOD double transgenic is combined with a homozygous Rag1^tm1Mom mutation, recombination of the endogenous TCR and immunoglobulin genes is prevented. As a result, mature T cells in these mice express only the BDC12-4.1 TCR. Further, approximately 50% of the TCR double transgenic, Rag1^tm1Mom homozygote mice develop diabetes by 30 weeks of age. Histopathology indicates severe insulitis and/or destruction of all insulin-producing cells (Jasinski et al 2006). This BDC12-4.1 TCR double transgenic, Rag1 deficient strain is useful for further studying the pathogenesis of insulin autoimmuni ..... For more information please see the full phenotype on the strain data sheet
014543	STOCK Hgf^{tm1.1(HGF)Aveo} Prkdc^scid/J	Repository- Live
	Mice homozygous for both the hHGFki and Prkdc^scid alleles, also called immunocompromised hHGFki mice, are viable and fertile. The hHGFki allele is a "humanized" knock-in mutation that replaces the mouse hepatocyte growth factor (HGF) coding region downstream of the signal sequence with the human HGF cDNA sequence. As a result, the endogenous mouse promoter drives expression of human HGF. While the human HGF activates both the human and murine form of its tyrosine kinase receptor (met proto-oncogene (MET; c-Met)), the murine HGF is unable to activate human MET. Mice homozygous for hHGFki express only the human form of HGF. In homozygous hHGFki mice, HGF expression from the knock-in allele is observed in developing embryo, as well as adult liver, kidney and lung. hHGFki homozygous mice exhibit an increase in serum HGF after clotting. Mice homozygous for the Prkdc^scid mutation exhibit T- and B-cell deficiency.
006770	STOCK Rag1^tm1Mom Tg(TIE2GFP)287Sato/J	Repository- Live
	To generate this double mutant strain, B6.Cg-Tg(TIE2GFP)287Sato/1J (Stock No. 004659) was crossed to C.129S7(B6)-Rag1^tm1Mom/J (Stock No. 003145). This mutant mouse strain may be useful in studies examining angiogenesis in transplanted tissues. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described for each single mutant. We will modify the strain description if necessary as published results become available.
016224	B6.129S(Cg)-Id2^tm2.1Blh/ZhuJ	Under Development - Now Accepting Orders
	The Id2-EGFP knockin allele was designed to both abolish inhibitor of DNA binding 2 (Id2) gene function and express enhanced green fluorescent protein (eGFP) from the Id2 promoter/enhancer elements. No mRNA or protein expression from the Id2-eGFP allele is observed. The donating investigator reports that homozygote mice mice are runted with defective lung alveolarization. Other organ systems have not been evaluated. However, Id2-eGFP homozygotes may be expected to exhibit the same phenotype as mice homozygous for other null mutations of this gene (including postnatal lethality and defects of the immune system, digestive tract, kidneys, adipose tissue and mammary gland development). The donating investigator also reports eGFP expression recapitulates the endogenous Id2 expression pattern. In the lungs, immunohistochemical detection of eGFP recapitulates the epithelial expression of the endogenous gene (distal tip lung epithelial multipotent precursor cells of the ..... For more information please see the full phenotype on the strain data sheet
017638	B6.129S4-Ccl7^tm1Ifc/J	Under Development - Now Accepting Orders
	In this strain a neo cassette replaces the entire coding region of the chemokine (C-C motif) ligand 7 (Ccl7) gene, abolishing gene function. CCL7, also known as MCP-3 (monocyte chemoattractant protein 3), directs the migration of monocytes to sites of inflammation through activation of the monocyte surface receptor CCR2 (chemokine (C-C motif) receptor 2). Homozygous CCL7 deficient mice are viable, fertile, and normal in size. These mice exhibit a 65% reduction of the 7/4 bri Ly-6G monocytes. These mice may be useful for studying the role of MCP-3 in monocyte recruitment and homeostasis.
017603	B6.129S6(129S4)-Tfpi^tm1.1Rdsi/J	Under Development - Now Accepting Orders
	The TFPI^Flox allele has loxP sites flanking exon 4 of the tissue factor pathway inhibitor gene [Tfpi]. Homozygous TFPI^Flox mice are viable and fertile with no observed abnormalities. When bred to mice that express Cre recombinase, the resulting offspring will have the sequences encoding the Kunitz 1 domain of TFPI protein (TFPI-K1) deleted in the cre-expressing tissues. This is designed to result in a K1-deleted form of TFPI containing the remainder of the TFPI protein (and to affect all K1-containing isoforms including TFPIα, TFPIβ, and TFPIγ). For example, when TFPI^Flox mice are bred to a strain expressing Cre recombinase in embryonic tissues (CMV-Cre; see Stock No. 006054), the resulting mice with pan deletion of the TFPI-K1 domain exhibit complete prenatal lethality; this is similar to mice homozygous for the TFPI knockout allele. In additio ..... For more information please see the full phenotype on the strain data sheet
016913	B6;129P2-Gmnn^tm1Tjm/J	Under Development - Now Accepting Orders
	These mice possess loxP sites flanking exons 5-7 of the geminin (Gmnn) gene. Homozygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Geminin is a regulatory protein involved in cell division and differentiation in the central nervous system, the axial skeleton, and the eye. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 5-7, encoding the dimerization domain and Cdt1 (chromatin licensing and DNA replication factor 1) binding site, deleted in the cre-expressing tissue. For example, when crossed to mice expressing cre driven by the myxovirus (influenza virus) resistance 1 (Mx1) promoter (see Stock No. 003556 for example), resulting offspring will lack Geminin in bone marrow cells. In such mice, red blood cell and leukocyte production is decreased and megakaryocyte production ..... For more information please see the full phenotype on the strain data sheet
012873	C.DDD-plt/NknoJ	Under Development - Now Accepting Orders
	Homozygous BALB/c-plt mice are viable and fertile, harboring the spontaneous plt (or "paucity of lymph node T cells") deletion of both the Ccl19 and Ccl21a loci on chromosome 4. Lack of expression of these two CCR7 receptor ligands in the secondary lymphoid organs results in abnormal leukocyte migration and impaired immune response. Specifically, homozygous mice have disrupted trafficking/homing of T cells and dendritic cells to lymphoid tissues. No reported abnormalities in B cell distribution/cellularity are reported for homozygous mice. Homozygous mice exhibit mature single-positive thymocyte arrest in the thymic cortex that results in defective formation of the medullary region of the thymus. Thymic export of T cells in these mice is compromised during the neonatal period but not in adulthood. While CCL21 expression is absent in lymphoid organs because of the Ccl21a deletion, CCL21 expression in non-lymphoid organs is observed because the upstre ..... For more information please see the full phenotype on the strain data sheet
003292	129S6/SvEvTac-Was^tm1Sbs/J	Cryopreserved - Ready for recovery
	WAS-deficient mice are viable and fertile. Mutant mice show normal lymphocyte development, serum immunoglobulin (Ig) levels and antibody responses. However, peripheral blood lymphocyte counts and platelet numbers are reduced in these mice. Development of chronic colitis is also observed. In vitro, WAS-deficient T cells show markedly impaired proliferative responses to anti-CD3e mediated stimulation. The Was gene is X-linked, so hemizygous males are WAS deficient.
012239	B6.129(Cg)-Cd44^tm1Hbg/SjJ	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected. Although lymphocyte development appears unremarkable, irregularities are observed in lymphocyte trafficking. Tail-injected lymphocytes derived from null animals exhibit an impaired ability to traffic to peripheral lymph nodes, and to a much greater degree, the thymus. Transcription and translation of the targeted allele subsequently lead to the synthesis of the lacZ protein under control of the 5' regulatory elements of the endogenous locus in all cells and tissues normally expressing one or several of the CD44 isoforms. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary f ..... For more information please see the full phenotype on the strain data sheet
003233	B6.129P2-Fas^tm1Osa/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Tnfrsf6^tm1Osa targeted mutation mice show hyperplasia in the liver in an age-dependent manner. Hepatocytes contain enlarged nuclei characteristic of senescent cells. Lymphadenopathy and splenomegaly in FAS deficient mice are evident at 8 weeks of age. The lymphnodes and spleen become progressively larger, becoming about 10 and 40 times larger than those of wildtype or heterozygotes at 16 weeks of age, respectively.
008313	B6.129P2-Hlx^tm1Rph/J	Cryopreserved - Ready for recovery
	Homozygous null mice have an embryonic lethal phenotype. Homozygous mice on the C57BL/6 and B6;129 mixed background fail to develop past embryonic days 15.5 due to impaired fetal hematopoiesis (anemia, hypoplastic and abnormal development of the liver, hypoplastic gut). Homozygous mice on the FVB/N background survive through embryonic day 18.5 and dead homozygote newborn pups are observed. Late gestation homozygous embryos on the FVB/N background are smaller than wildtype littermates, pale, hydropic (subcutaneous fluid ballooning skin), and have impaired neural crest cell and enteric neuron migration from the stomach to intestine. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Naive CD4 T cells from heterozygotes exhibit increased responsiveness to IL-4, resulting in differentiation of more Th2 cells. This mutant mouse strain may be useful in studies of liver and gastrointe ..... For more information please see the full phenotype on the strain data sheet
008171	B6.129P2-Maea^Gt(XG702)Byg/LlpJ	Cryopreserved - Ready for recovery
	Homozygotes die after embryonic day 19.5 and before birth. These homozygotes are smaller than normal from embryonic day 14.5 on, have increased nucleated, immature erythrocytes in the peripheral blood, lack erythroblastic islands in the liver, and have only a quarter to a third the normal number of F4/80 staining macrophages in the liver. These macrophages are morphologically abnormal and fail to facilitate erythroblast enucleation.
002463	B6.129S-Itga4^tm1Hyn/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Itga4^tm1Hyn targeted mutation die during embryonic development. Homozygous mutant embryos fail to fuse the allantois with the chorion during placentation. There is a defect in the epicardium and coronary vessels results in in utero cardiac hemorrhage; also known as CD49D, VLA-4.
005669	B6.129S-Runx1^tm1Spe/J	Cryopreserved - Ready for recovery
	Heterozygous mice are viable, fertile, devoid of hemorrhagic lesions, and exhibit mild hematopoietic impairment. Mice that are homozygous for the targeted mutation have an embryonic lethal phenotype; animals are alive at embryonic day 11.5, but start dying at embryonic day 12.5. Embryos exhibit extensive hemorrhagic lesions in the central nervous system including the intraventricular regions and metencephalon as well as segmental bleeds at the VII-VIII cranial nerve complex, cervical, thoracic, and caudal regions. At embryonic day 10.5, symmetrical and bilateral necrosis preceding hemorrhage is observed in homozygotes. Homozygous disruption of the endogenous gene completely blocks definitive erythropoiesis, myelopoiesis, and lymphopoiesis. This mutant may be useful in leukemia studies as disruption of the human homolog of this gene is associated with many different leukemias.
005963	B6.129S1-Csf2rb2^tm1Cgb Csf2rb^tm1Clsc/J	Cryopreserved - Ready for recovery
	Mice homozygous at both loci are viable and fertile with no behavioral abnormalities. Steady state hematopoiesis is normal. Bone marrow from homozygous mice fail to exhibit any cellular responses to GM-CSF, IL-5, or IL-3. Like the similar strain (Stock No. 005940; Csf2rb^tm1Cgb), double homozygous mice exhibit eosinopenia, increased surfactant accumulation in lung tissue and pulmonary alveolar proteinosis (PAP), infection resistance, and attenuated tissue repair after injury. This mutant may be useful in studies of PAP, lung physiology and disease, surfactant homeostasis and metabolism, innate immunity, cytokine signaling, myoproliferative disease, hematopoietic cell populations requiring IL-3, GM-CSF, or IL-5 for development and function, and models of ischemic, traumatic, toxic, and inflammatory injuries.
005940	B6.129S1-Csf2rb^tm1Cgb/J	Cryopreserved - Ready for recovery
	Homozygous mice are viable and fertile with no behavioral abnormalities. In response to GM-CSF, bone marrow and splenocytes from homozygous mice fail to exhibit proliferation, enhanced survival in vitro, or synergistic interaction with M-CSF. They also fail to proliferate in response to IL-5. IL-3 binding and responses are unaffected. Cell composition in thymus, spleen, bone marrow, and lymph node is not significantly altered. Circulating eosinophils are dramatically reduced in blood with lesser reduction in bone marrow and tissues. Homozygous mice develop pulmonary peribronchovascular lymphoid infiltrates and areas resembling pulmonary alveolar proteinosis (PAP). Consistent with this, mutant mice have greatly increased surfactant protein-B and D accumulation in lung/airway tissue, no attenuation of saturated phosphatidylcholine with advancing age, and high levels of GM-CSF in bronchoaveolar lavage fluid. Homozygous mice are resistant to intradermal Leishmania major infection an ..... For more information please see the full phenotype on the strain data sheet
008439	B6.129S2-Sele^tm1Hyn Sell^tm1Hyn Selp^tm1Hyn/J	Cryopreserved - Ready for recovery
	Mice that are homozygous null for the Sele, Sell and Selp genes are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities at birth. As mice mature, however, they become susceptible to mucocutaneous infections that eventually lead to death. No Sele, Sell or Selp gene products (mRNA or protein) are detected. Leukocytes from these mice exhibit a deficiency in the ability to interact with, and roll along, the venular wall endothelium. This deficiency in the crucial first step of leukocyte recruitment to surrounding tissues in response to infection or injury contributes to an elevated leukocyte count in the peripheral blood. Delays in neutrophil and eosinophil recruitment to the peritoneum in response to thioglycollate and ragweed allergen, respectively, have been observed, specifically. These mice are suitable for use in research applications studying leukocyte homeostasis, infectious diseases and inflam ..... For more information please see the full phenotype on the strain data sheet
008437	B6.129S2-Sele^tm1Hyn Selp^tm1Hyn/J	Cryopreserved - Ready for recovery
	Mice homozygous for both the Sele^tm1Hyn Selp^tm1Hyn mutations are viable and fertile. They are characterized by leukocytosis, spontaneous bacterial infections, dermatitis and defective leukocyte recruitment in many models of inflammation. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
008434	B6.129S2-Sele^tm2Hyn/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Sele^tm2Hyn targeted mutation are viable and fertile. Homozygous mutant mice show only subtle defects in leukocyte recruitment, unless P-selectin (Selp) is also ablated or blocked with antibody. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
010572	B6.129S2-Tnfsf13b^tm1Msc/J	Cryopreserved - Ready for recovery
	Homozygous (BAFF^-/- or BAFF KO) mice are viable and fertile. The BAFF knockout mutation has a tailless human CD2 reporter gene inserted into the Tnfsf13b (BAFF) locus that abolishes endogenous BAFF expression. Homozygous mice exhibit abnormal B cell development and function, resulting from significant loss of mature B cell (B220⁺) populations in lymph nodes, peripheral blood and bone marrow, as well as attenuated antibody responses to both T cell-dependent and T cell-independent type II antigens. Homozygous also have splenic deficiencies (mass, marginal zone B cells and follicular B cells), and decreased total serum immunoglobulin in each subclass (with the exception of immunoglobulin A [IgA] which was only moderately reduced). No loss of marrow pre-B cells, marrow pro-B cells, or CD3⁺ T cells are reported with BAFF-deficiency. Heterozygous mice have moderately reduced serum IgG subclasses and IgM. These BAFF-mutant mice may be useful in studyin ..... For more information please see the full phenotype on the strain data sheet
006198	B6.129S4-Matk^tm1Sor/J	Cryopreserved - Ready for recovery
	Homozygotes are viable and fertile with no behavioral abnormalities. The donating investigator reports homozygous mutants have no endogenous protein expression. Homozygous mice have an approximately 2-fold increase in the primitive hematopoietic stem cell population SPKLS (c-Kit⁺, Lin^-, Sca-1⁺ in combination with side population cells). Homozygous deficiency also leads to the hyperproliferation of pre-B cells in the presence of Interleukin-7, and impaired IFN-gamma production in lymph and spleen cells upon in vivo antigen challenge. These mutant mice may be useful in studying tyrosine phosphorylation of hematopoietic cells, primitive/early hematopoietic populations, immune cell signaling, and regulation of immunological responses.
006447	B6.129S6(CBA)-Cebpa^tm1Dgt/J	Cryopreserved - Ready for recovery
	Mice carrying this C/EBPalpha "floxed" allele (C/EBPalphaF) are viable and fertile. The floxed allele functions similarly to the wildtype allele. In mice homozygous for C/EBPalpha^F and expressing an interferon-inducible Cre recombinase (introduced by breeding to a cre-expressing strain; see Stock No. 003556), C/EBPalpha activity is disrupted, leading to defective myeloid cell development, increased hematopoietic stem cell repopulating activity, and significantly increased myeloblast population in the bone marrow compartment. In combination with an appropriate Cre transgenic strain, these mutant mice may be useful in studies of hematopoietic cell (e.g. myeloid and basophil progenitor cell) development and function, cancer (e.g. acute myeloid leukemia), and alveolar cell differentiation.
004197	B6.129S6-Rac2^tm1Mddw/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable, fertile, and normal in size but exhibit phagocytic immunodeficiency. No endogenous gene product (mRNA or protein) was detected by Northern blot analysis, RT-PCR or Western blot analysis. The Rac proteins are a subclass of the Rho family of GTPases, and are involved in actin cytoskeletal organization in cell movement, cell proliferation, kinase signaling pathways, and in superoxide production in phagocytic cells. Neutrophils and mast cells derived from homozygous mice display abnormal actin-based functions: cytoskeleton remodeling ability, adhesion, migration, degranulation, and phagocytosis. Diminished superoxide production in response to some agonists, and reduced total number of leukocytes and neutrophils in peritoneal exudate is observed. As result of functional deficiencies in neutrophil and mast cell populations, these mutant mice are more vulnerable to invasive infection. Slowed growth of mast cells, accompanying redu ..... For more information please see the full phenotype on the strain data sheet
003863	B6.129S6-Tapbp^tm1Luc/J	Cryopreserved - Ready for recovery
	Mice that are homozygous null for the Tapbp gene are viable and fertile. No Tapbp gene product is detected. Tapbp is an integral component of the MHC class I peptide loading complex. Expectedly, mice that are homozygous null for tapasin fail to assemble loading complexes. Overall expression of surface MHC class I expression is reduced. Although some class I molecules are able to translocate to the cell surface, they are unable to do so in association with peptide antigen. Antigen presenting cells from null animals had a slightly reduced ability to stimulate CD8⁺ T cells. A more significant defect is observed in the ability to present foreign antigen. CTL responses are differentially affected. Significant defects in positive and negative intrathymic selection are also observed.
004341	B6.129X-Cxcr4^tm1Qma/J	Cryopreserved - Ready for recovery
	Mice that are homozygous null for the Cxcr4 gene die perinatally, with ~30% dying by embryonic day 18.5. Viable embryos are slightly smaller than wild type mice and exhibit vascular congestion in the kidneys, interstitial hemorrhages, and abnormalities in bone marrow and cerebellum. Homozygote embryos also show reduced B-lymphopoiesis, reduced myelopoiesis in fetal liver and an absence of myelopoiesis in bone marrow. Histological examination reveals a distorted architecture in the tissues if the cerebellum, featuring an attenuated external granule cell layer and an ectopic placement of Purkinje cells. Cxcr4 encodes a receptor commonly called CXCR4, the ligand of which is the chemokine stromal cell-derived factor 1 (SDF-1), an important regulator of hematopoietic cell development, migration and proliferation. CXCR4 also functions as a coreceptor for the entry of T-tropic strains of HIV-1 into CD4⁺ T cells. In an attempt to offer alleles on well-charac ..... For more information please see the full phenotype on the strain data sheet
000204	B6.C3Rl-Lyst^bg/J	Cryopreserved - Ready for recovery
	Mice homozygous for the beige spontaneous mutation (Lyst^bg) are characterized by a condition that closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syngeneic tumor cells grow better in beige mice than in l ..... For more information please see the full phenotype on the strain data sheet
006230	B6.Cg-Cebpa^tm1Dgt Tg(Mx1-cre)1Cgn/J	Cryopreserved - Ready for recovery
	Mice homozygous for this C/EBPalpha "floxed" allele (C/EBPalpha^F) and hemizygous for the Mx1-cre transgene are viable and fertile, and exhibit no abnormalities in the hematopoietic system. In the absence of cre expression, the C/EBPalpha^F allele functions similarly to the wildtype allele. Mx1-Cre transgene expression can be induced by administration of either interferon (alpha or beta) or synthetic double-stranded RNA (such as poly I:C), leading to deletion of the "floxed" gene. Following 3-4.5 weeks of poly I:C treatment, deletion efficiency is greater than 95% in hematopoietic tissues, and C/EBPalpha protein is undetectable in bone marrow. These poly I:C-treated, mice have defective myeloid cell development, increased hematopoietic stem cell repopulating activity, and a significantly increased myeloblast population in the bone marrow compartment. These mutant mice may be useful in studies of hematopoietic cell (e.g. myeloid and basophil progenitor cell) d ..... For more information please see the full phenotype on the strain data sheet
005912	B6.Cg-Il10^tm1Cgn (D3Mit49-D3Mit348)/Lt	Cryopreserved - Ready for recovery
	Homozygous mice are IL10-deficient and develop spontaneous colitic lesions in the cecum and large intestine as early as 6-8 weeks of age. The severity and age of onset of colitis varies with the donor type and location of the cytokine deficiency colitis susceptibility 1 (Cdcs1) interval. Generally, the C3H/HeJBir region encompassed by D3Mit348 through D3Mit254 (127.7-132.5 megabases) confers increased colitis susceptibility on the B6.129P2-Il10^tm1Cgn background (Beckwith J, et al., 2005). Mice on the B6.129P2-Il10^tm1Cgn background are prone to rectal prolapse particularly when carrying susceptibility alleles from Chromosome 3. Granulocyte populations in peripheral blood increase upon lesion development and provide a robust non-lethal assessment of colitis severity.
006194	B6.Cg-Polq^tm1Jcs/J	Cryopreserved - Ready for recovery
	Mice homozygous for this targeted mutation are viable and fertile, with no gross anatomical or behavioral abnormalities. Homozygotes exhibit significant spontaneous and induced genome instability, and have a 60-80% reduction in somatic hypermutation in B cells. Mutant mice may be useful in studies related to DNA recombination and repair, translesion polymerases, genomic instability, and the mechanisms for generating immune diversity (e.g. somatic hypermutation and immunoglobulin gene class switching).
004201	B6.Cg-Selplg^tm1Fur/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No targeted allele product (mRNA or protein) is detected by Northern blot or immunoassay. Mutant mice exhibit mild neutrophilia. Impaired early neutrophil migration in thioglycolate-induced peritonitis is followed by a delayed recovery to nearly normal levels. Although early trauma-induced leukocyte adhesion and migration is greatly reduced and in vivo leukocyte rolling (leukocyte-endothelial cell interaction) in postcapillary venules is severely decreased, cytokine-induced/E selectin-mediated leukocyte rolling is only slightly reduced in the mutant mice. This mutant mouse strain represents a model that may be useful in studies of leukocyte adhesion and migration in the inflammatory response.
004338	B6;129-E2f2^tm1Zubi/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable and normal in size. No gene product, mRNA or protein, was detected. At age 15 months mutant mice have a 27% survival rate due to diffuse autoimmune disease that resembles systemic lupus erythematosus (SLE). The phenotype includes splenomegaly by 8-12 weeks of age, glomerulonephritis, accumulated inflammatory infiltrates in the lung, liver, and skin abnormalities such as hair loss, skin wounds, erythema. Anti-dsDNA antibodies are detected in the serum. There are an increased number of mature CD8+ thymocytes and an abnormal accumulation of CD8+ Cd44high Cd69- T effector/memory cells that are autoreactive in peripheral lymphoid organs. E2F2 deficient mice appear to have normal negative selection of thymocytes but demonstrate defects in peripheral tolerance of T lymphoctes (especially Cd8+ T cells) leading to progressive autoimmune disease. This mutant mouse strain may be useful in studies of autoimmunity and may serve as model ..... For more information please see the full phenotype on the strain data sheet
002121	B6;129P-Tcrb^tm1Mom Tcrd^tm1Mom/J	Cryopreserved - Ready for recovery
	Mice homozygous for both the Tcrb^tm1Mom and the Tcrd^tm1Mom targeted mutations express no alpha beta T-cell receptor nor any gamma delta T-cell receptor. Under certain housing conditions homozygous mutant mice develop mild inflammatory bowel disease.
002117	B6;129P2-Tcrb^tm1Mom/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Tcrb^tm1Mom targeted mutation are viable and fertile. Mice are deficient in alpha beta T-cell receptor. The total number of cells in the thymus is ~8% that of wildtype; CD4⁺CD8⁺ cells ~6% of wildtype. The proportion of CD4^-CD8- (IL2 receptor positive) cells increases to about 50% of the total cell number. Alpha beta thymocyte differentiation is blocked at an earlier stage than the Tcra^tm1Mom strain. There is normal differentiation of gamma delta thymocytes. Mice may develop inflammatory bowel disease beginning at ~4-6 months of age.
002119	B6;129P2-Tcrd^tm1Mom/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Tcrd^tm1Mom targeted mutation are viable and fertile. Gamma delta T-cell receptor expression is deficient in all adult lymphoid and epithelial organs. There is normal development of the alpha beta T-cell lineage. Patterns of CD4⁺CD8^- and CD4^-CD8⁺ alpha beta T-cells are apparently normal. Mice do not develop inflammatory bowel disease.
002536	B6;129S-Btk^tm1Wk/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Btk^tm1Wk targeted mutation are viable and fertile. Homozygous mutant mice show defects in B-cell maturation and activation. This strain has the same phenotype as the spontaneous X-linked immune deficiency mutation (CBA/CaHN-Btk^xid/J; Stock No. 001011). See Inbred Strain listing.
003807	B6;129S-Sele^tm1Hyn Sell^tm1Hyn Selp^tm1Hyn/J	Cryopreserved - Ready for recovery
	Mice that are homozygous null for the Sele, Sell and Selp genes are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities at birth. As mice mature, however, they become susceptible to mucocutaneous infections that eventually lead to death. No Sele, Sell or Selp gene products (mRNA or protein) are detected. Leukocytes from these mice exhibit a deficiency in the ability to interact with, and roll along, the venular wall endothelium. This deficiency in the crucial first step of leukocyte recruitment to surrounding tissues in response to infection or injury contributes to an elevated leukocyte count in the peripheral blood. Delays in neutrophil and eosinophil recruitment to the peritoneum in response to thioglycollate and ragweed allergen, respectively, have been observed, specifically. These mice are suitable for use in research applications studying leukocyte homeostasis, infectious diseases and inflam ..... For more information please see the full phenotype on the strain data sheet
002916	B6;129S2-Sele^tm1Hyn Selp^tm1Hyn/J	Cryopreserved - Ready for recovery
	Mice homozygous for both the Sele^tm1Hyn Selp^tm1Hyn mutations are viable and fertile. They are characterized by leukocytosis, spontaneous bacterial infections, dermatitis and defective leukocyte recruitment in many models of inflammation.
002115	B6;129S2-Tcra^tm1Mom/J	Cryopreserved - Ready for recovery
	Mice homozygous mice for the Tcra^tm1Mom targeted mutation are viable and fertile. They are deficient in the alpha beta T-cell receptor. The thymus is devoid of CD4⁺CD8^- and CD4^-CD8⁺ cells. Normal numbers of CD4⁺CD8⁺ cells are retained without the IL2 receptor. There are normal numbers of CD4^-CD8^- cells. ~1% of the thymocytes express the gamma delta TCR. Mice may develop inflammatory bowel disease beginning at ~4-6 months of age.
003542	B6;SJL-Tg(FCGR2A)11Mkz/J	Cryopreserved - Ready for recovery
	Studies of the immune destruction of blood cells, such as platelets in immune thrombocytopenia, serve as a model for exploring the pathophysiology of these disorders. In general, mice lack the genetic equivalent of human FCGR2A, which is the FC receptor for IgG. This strain expresses human FCGR2A on mouse platelets and macrophages at levels equivalent to that observed in human cells. Antibody-mediated thrombocytopenia is significantly more severe than that observed in wild type mice. There is no phenotype in the absence of anti-platelet antibodies.
000604	B6C3 a/A-T(10;13)199H +/+ Lyst^bg-J/J or Lyst^bg-2J/J	Cryopreserved - Ready for recovery

007848	BXSB.129P2(Cg)-Tcra^tm1Mjo/TheoJ	Cryopreserved - Ready for recovery
	Male mice on the BXSB recombinant inbred genetic background (see Stock No. 000740) develop spontaneous autoimmune disease closely resembling the human disease systemic lupus erythematosus (SLE), including moderate lymph node and spleen enlargement, hemolytic anemia, hypergammaglobulinemia, and immune complex glomerulonephritis. This autoimmune phenotype is associated with at least six non-MHC loci (the Y chromosome linked Yaa, Bxs1-4 on chromosome 1 and Bxs6 on chromosome 13) and defined by increased homeostatic proliferation of self-reactive T cells. Because these BXSB-Tcrα^-/- mice are homozygous for the Tcrα targeted mutation, they lack αβ⁺ T cells and do not develop spontaneous lupus symptoms. These BXSB-Tcrα^-/- mice may be useful for adoptive transfer experiments for studying the role of T cells in systemic autoimmunity and lupus.
002229	C.129P2(B6)-Il2^tm1Hor/J	Cryopreserved - Ready for recovery
	Homozygous mutant mice for the Il2^tm1Hor targeted mutation show no apparent deficit in thymocyte differentiation or selection, types and numbers of T cells from spleens and lymph nodes are comparable to those of wildtype. They do have an impaired response to polyclonal T cell activators in the absence of additional IL2, deficits in their helper function and a reduction in natural killer cell activity. There is significant pre-weaning and post-weaning loss of homozygotes on the C3H/HeJCrlBR and C57BL/6J genetic backgrounds. In addition, homozygous mice develop inflammatory bowel disease between 6 and 15 weeks of age and reportedly die within 10-25 weeks under conventional housing conditions. Homozygotes on the C57BL/6J genetic background show an atrophied pancreas with apparently intact islets. Homozygotes on the BALB/c genetic background do not develop inflammatory bowel disease symptoms but rather die 3-5 weeks postnatally of a form of hemolytic anemia. For a more de ..... For more information please see the full phenotype on the strain data sheet
008440	C.129S2(B6)-Sele^tm1Hyn Sell^tm1Hyn Selp^tm1Hyn/J	Cryopreserved - Ready for recovery
	Mice that are homozygous null for the Sele, Sell and Selp genes are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities at birth. As mice mature, however, they become susceptible to mucocutaneous infections that eventually lead to death. No Sele, Sell or Selp gene products (mRNA or protein) are detected. Leukocytes from these mice exhibit a deficiency in the ability to interact with, and roll along, the venular wall endothelium. This deficiency in the crucial first step of leukocyte recruitment to surrounding tissues in response to infection or injury contributes to an elevated leukocyte count in the peripheral blood. Delays in neutrophil and eosinophil recruitment to the peritoneum in response to thioglycollate and ragweed allergen, respectively, have been observed, specifically. These mice are suitable for use in research applications studying leukocyte homeostasis, infectious diseases and inflam ..... For more information please see the full phenotype on the strain data sheet
008438	C.129S2(B6)-Sele^tm1Hyn Selp^tm1Hyn/J	Cryopreserved - Ready for recovery
	Mice homozygous for both the Sele^tm1Hyn Selp^tm1Hyn mutations are viable and fertile. They are characterized by leukocytosis, spontaneous bacterial infections, dermatitis and defective leukocyte recruitment in many models of inflammation. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
002964	C.129S2-Itgae^tm1Cmp/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the Itgae^tm1Cmp targeted mutation are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. No Itgae expression is detected in intraepithelial lymphocytes by FACS analysis or on TGF-beta1-treated splenocytes by immunoprecipitation. Homozygous null mice exhibit reduced numbers of intestinal intraepithelial lymphocytes and lamina propria lymphocytes.
007680	C.129X1-Il4ra^tm1Tch/J	Cryopreserved - Ready for recovery
	Mice homozygous for this "IL4Rα Y500F" mutant allele are viable and fertile. The mice express a mutant IL4Rα chain with a phenylalanine substitution at the proximal tyrosine residue (Y500F) in the cytoplasmic tail. This residue is a critical component of the insulin/interleukin-4 receptor (I4R) motif, and is required for binding by phosphotyrosine-binding domain (PTB) adaptor proteins and for initiating subsequent downstream signaling cascades in response to IL-4. Allele-specific PCR verifies the amino acid substitution. The Y500F mutation abrogates insulin receptor substrate-2 (IRS-2) phosphorylation, and impairs IL-4-induced CD4+ lymphocyte proliferation with no reported effect on Stat6 activation, IL-4-responsive gene product up-regulation, or Th cell differentiation under Th2 polarizing conditions. In vivo, the Y500F mutation is associated with increased allergen-induced IgE production, airway hyper-responsiveness (AHR), tissue eosinophilia, goblet cell metaplasi ..... For more information please see the full phenotype on the strain data sheet
007746	C.129X1-Il4ra^tm2Tch/J	Cryopreserved - Ready for recovery
	Mice homozygous for this IL4Rα Q576R polymorphic allele (Il4ra^R576) are viable and fertile. The mutation introduces an arginine substitution at glutamine 576 (Q576R) in the protein sequence. This polymorphism is associated with severe asthma susceptibility and rapid smoking-associated lung function decline in human populations. Allele-specific PCR verifies the amino acid substitution. Homozygous mice exhibit heightened IgE responses in vivo, and augmented antigen- and IL-13-driven allergic airway inflammation. T cells from homozygotes show increased production of IL-4 in a Th2 polarized milieu. The R576 substitution is associated with enhanced Erk kinase activation with no reported effect on the activation of other canonical IL-4Rα-coupled pathways. These Il4ra^R576 mutant mice may be useful in immunological studies of mitogenic signal transduction, specifically antigen-specific antibody responses, allergic airway inflammation, atop ..... For more information please see the full phenotype on the strain data sheet
012709	C.129X1-Il4ra^tm3.1Tch/J	Cryopreserved - Ready for recovery
	Mice homozygous for this Il4ra^F709 (IL-4Rα Y709F) polymorphic allele are viable and fertile. The mutation introduces a tyrosine to phenylalanine amino acid substitution at codon 709 (Y709F) within the canonical immunoreceptor tyrosine-based inhibitory motif (ITIM) sequence near the carboxyl-terminus of the protein. This Y709F polymorphism prevents ITIM phosphorylation and inhibit the binding of regulatory phosphatases (including Src homology 2 domain-containing protein tyrosine phosphatase 1 [SHP-1]), resulting in enhanced receptor signaling. Allele-specific PCR verifies the Y709 to F709 codon substitution. Homozygous mice exhibit enhanced phosphorylation of signal transducer and activator of transcription 6 (STAT6) in B cells following IL-4 treatment, and increased serum concentrations of total IgE and ovalbumin (OVA)-specific IgE after immunization with OVA/alum. Il4ra^F709/F709 mice have increased allergic airway inflammation (peribronchial a ..... For more information please see the full phenotype on the strain data sheet
004364	C.Cg-Tcra^tm1Mom Tcrb^tm1Mom/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable and fertile. Mutant mice display early stage arrest of alpha beta thymocyte differentiation. Mice may develop inflammatory bowel disease.
002045	C.SJL-Tcra^c/SlkJ	Cryopreserved - Ready for recovery

002047	C.SJL-Tcrb^a Tcra^c/SlkJ	Cryopreserved - Ready for recovery

002228	C3.129P2(B6)-Il2^tm1Hor/J	Cryopreserved - Ready for recovery
	Homozygous mutant mice for the Il2^tm1Hor targeted mutation show no apparent deficit in thymocyte differentiation or selection, types and numbers of T cells from spleens and lymph nodes are comparable to those of wildtype. They do have an impaired response to polyclonal T cell activators in the absence of additional IL2, deficits in their helper function and a reduction in natural killer cell activity. There is significant pre-weaning and post-weaning loss of homozygotes on the C3H/HeJCrlBR and C57BL/6J genetic backgrounds. In addition, homozygous mice develop inflammatory bowel disease between 6 and 15 weeks of age and reportedly die within 10-25 weeks under conventional housing conditions. Homozygotes on the C57BL/6J genetic background show an atrophied pancreas with apparently intact islets. Homozygotes on the BALB/c genetic background do not develop inflammatory bowel disease symptoms but rather die 3-5 weeks postnatally of a form of hemolytic anemia. For a more de ..... For more information please see the full phenotype on the strain data sheet
008228	C3.129S7(B6)-Ifng^tm1Ts/J	Cryopreserved - Ready for recovery
	Leukocytes do not respond to and Th1 cells are not activated by skin grafts in homozygous mice. Homozygotes are resistant to experimentally induced alopecia areata with diminished T cell infiltration in skin and reduced MHC class I and II molecule expression in the hair follicle infrainfundibular site. No gene product (protein) is detected by ELISA analysis of splenocyte supernatants from homozygous animals. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of immune response, inflammation and autoimmunity.
000509	C3.Cg-Lyst^bg-2J/J	Cryopreserved - Ready for recovery
	Mice homozygous for the beige 2J spontaneous mutation (Lyst^bg-2J) display characteristics very similar to the original beige mutation (Lyst^bg). The mouse phenotype closely resembles Chediak-Higashi syndrome in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to a ..... For more information please see the full phenotype on the strain data sheet
003968	C3Bir.129P2(B6)-Il10^tm1Cgn/LtJ	Cryopreserved - Ready for recovery
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full phenotype on the strain data sheet
007707	C57BL/6-Itgb7^tm1Mshi/J	Cryopreserved - Ready for recovery
	Mice homozygous for this β₇ (D146A) targeted mutation are viable and fertile. DNA sequencing confirms an aspartate (D) to alanine (A) substitution at position 146 of the targeted β₇ integrin gene. As such, homozygotes have a mutant ADMIDAS (adjacent to metal ion-dependent adhesion site) cation binding/exchange site in the β₇ integrin head (A-domain). The resulting imbalance between the non-adhesive and adhesive states of leukocyte integrins skews toward a persistently adhesive state. Homozygous mutants exhibit impaired leukocyte migration, perturbed lymphocyte trafficking in the gut, and reduced T- and B-cell numbers in small/large bowel and gut-associated lymphoid tissues (less T-cells in Peyer's patches (PP), fewer intraepithelial lymphocyte (IEL) and lamina propria lymphocyte (LPL) compartments in the small intestine; and less B-cells in PP and the large intestine). In addition, CD4⁺CD45RB^high T cells isolated fro ..... For more information please see the full phenotype on the strain data sheet
005342	C57BL/6J-Il7^hlb368/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified an 8 week old male (born 4/7/2003) with a CBC of 1.50 x 103 WBC/ul (84% lower than controls); testing two weeks later produced a result of 2.51 WBC/ul (74% lower than controls). This mutant mouse strain may be useful in studies of leukopenia.
000529	C57BL/6J-Lbr^ic-J/J	Cryopreserved - Ready for recovery
	Lbr^ic-J/Lbr^ic-J homozygotes can be identified at 2 weeks of age due to sparse fur and at 3-4 weeks of age scales develop on the tail and, to a lesser degree, on the trunk. These mutants are smaller than their wild type siblings. The mutants develop mild epidermal hyperplasia with orthokeratotic hyperkeratosis and dilation of the piliary canals. Homozygotes have an increased incidence of syndactyly and hydrocephaly, and a high prenatal mortality rate. Aberrant morphology of nuclear heterochromatin occurs in lymphocytes, neutrophils, eosinophils, intestinal epithelium, and cerebellar granule cells. Electron microscopy reveals clumps of heterochromatin at the periphery of the nucleus within splenic lymphocytes. These mice are a model for Pelger-Huet anomaly, which is associated with mutations in LBR, although the skin pathology is specific to the mouse mutation. (Eicher, 1976; Hoffmann et al., 2002; Shultz et al., 2003.)
005579	C57BL/6J-Lta^hlb382/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3)identified a non-fasted female (born 10/9/2003) with an increased white blood cell count of 15.39 x 103 cells/ul, which is approximately 92% higher than controls. This mutant mouse strain may be useful in studies of leukocytosis.
005496	C57BL/6J-hlb385/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 7 week old female (born 12/13/2003) with a complete blood count (CBC) of 3.2 x 103 white blood cells (WBC)/ul, approximately 60% lower than controls. Retesting 2 weeks later confirmed the phenotype. This mutant mouse strain may be useful in studies of leukopeniia.
008312	CBy.129P2(B6)-Tcrd^tm1Mom/SzJ	Cryopreserved - Ready for recovery
	Mice homozygous for the Tcrd^tm1Mom targeted mutation are viable and fertile. Gamma delta T-cell receptor expression is deficient in all adult lymphoid and epithelial organs. There is normal development of the alpha beta T-cell lineage. Patterns of CD4⁺CD8^- and CD4^-CD8⁺ alpha beta T-cells are apparently normal. Mice do not develop inflammatory bowel disease. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
007081	CByJ.129P2(B6)-Tcrb^tm1Mom/J	Cryopreserved - Ready for recovery

003448	CByJ.129P2(B6)-Tcrd^tm1Mom/Sz	Cryopreserved - Ready for recovery
	Mice homozygous for this targeted mutation are viable and fertile. Gamma delta T-cell receptor expression is deficient in all adult lymphoid and epithelial organs. There is normal development of the alpha beta T-cell lineage. Patterns of CD4+CD8- and CD4-CD8+ alpha beta T-cells are apparently normal. Mice do not develop inflammatory bowel disease. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
008338	CByJ.B6(Cg)-Rag2^tm1Cgn/J	Cryopreserved - Ready for recovery
	Mice homozygous for the RAG-2^fl allele are viable and fertile, with loxP sites flanking exon 3 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have this region (coding for the entire RAG-2 protein) deleted in the cre-expressing tissue(s). These RAG-2^fl mice may be useful in generating conditional mutations for studying the role of RAG-2 in B and T cell development (including cancer and toxicology research as a xenograft/transplant host), T and B cell receptor (V(D)J) recombination, hematopoiesis, hematology, immunology, and inflammation research. For example, when bred to a strain with inducible Cre recombinase expression in liver and lymphocytes (see Stock No. 003556), this mutant mouse strain may be useful in studies of B and T cell development. In an attempt to offer alleles on well-characterized or multiple genetic background ..... For more information please see the full phenotype on the strain data sheet
007225	FVB.129(B6)-Usp18^tm1Dzh/J	Cryopreserved - Ready for recovery
	Homozygous Usp18 (or Ubp43) mutant mice on the FVB/N genetic background are viable and fertile, exhibiting none of the severe neurologic disorders that lead to embryonic lethality or early death reported for Ubp43-deficient mice on a C57BL/6 or mixed B6;129 genetic background. In contrast to wildtype mice, thymi from homozygous mice injected with LPS exhibit no protein from the targeted gene. Expression of the lacZ cassette is observed in both heterozygous and homozygous brain tissues. Homozygous mice are hypersensitive to type I interferon (IFN) and undergo apoptosis upon IFN stimulation. Ubp43-deficiency results in enhanced and prolonged STAT1 phosphorylation, DNA binding, and increased induction of hundreds of interferon stimulated genes (ISGs). Homozygous mice exhibit greater resistance to the cytopathic effects caused by a number of viruses (including lymphocytic choriomeningitis virus (LCMV), vesicular stomatitis virus (VSV), and Sindbis virus (SNV)). Ubp43-defici ..... For more information please see the full phenotype on the strain data sheet
008315	FVB.129P2(Cg)-Hlx^tm1Rph/J	Cryopreserved - Ready for recovery
	Homozygous null mice have an embryonic lethal phenotype. Homozygous mice on the C57BL/6 and B6;129 mixed background fail to develop past embryonic days 15.5 due to impaired fetal hematopoiesis (anemia, hypoplastic and abnormal development of the liver, hypoplastic gut). Homozygous mice on the FVB/N background survive through embryonic day 18.5 and dead homozygote newborn pups are observed. Late gestation homozygous embryos on the FVB/N background are smaller than wild-type littermates, pale, hydropic (subcutaneous fluid ballooning skin), and have impaired neural crest cell and enteric neuron migration from the stomach to intestine. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Naive CD4 T cells from heterozygotes exhibit increased responsiveness to IL-4, resulting in differentiation of more Th2 cells. This mutant mouse strain may be useful in studies of liver and gastrointestin ..... For more information please see the full phenotype on the strain data sheet
006202	FVB/N-Tg(tetO-BCR/ABL1)2Dgt/J	Cryopreserved - Ready for recovery
	Hemizygotes are viable, fertile, normal in size, and do not display any behavioral abnormalities. Transgene expression is directed by the tetracycline-responsive element (TRE; tetO). When hemizygotes are bred with another transgenic mouse expressing either reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the regulation of tissue-specific promoters , BCR-ABL1 fusion protein expression can be regulated in the appropriate tissue of the bitransgenic offspring with the tetracycline analog, doxycycline. These mice originally were designed to be bred with transgenic mice harboring a Tal1-tTA transgene (see Stock No. 006209), creating double transgenic offspring as a model for studies of the Philadelphia chromosome and inducible chronic myeloid leukemia. When bred to a strain expressing tTA in the epithelial cells of secretory organs and skin (see Stock ..... For more information please see the full phenotype on the strain data sheet
000494	J.Cg-Oca2⁺ Tyr⁺ Lyst^bg/J	Cryopreserved - Ready for recovery
	Mice homozygous for the beige spontaneous mutation (Lyst^bg) are characterized by a condition that closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syngeneic tumor cells grow better in beige mice than in l ..... For more information please see the full phenotype on the strain data sheet
003234	MRL.129P2(B6)-Fas^tm1Osa/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Tnfrsf6^tm1Osa targeted mutation mice show hyperplasia in the liver in an age-dependent manner. Hepatocytes contain enlarged nuclei characteristic of senescent cells. Lymphadenopathy and splenomegaly in FAS deficient mice are evident at 8 weeks of age. The lymphnodes and spleen become progressively larger, becoming about 10 and 40 times larger than those of wildtype or heterozygotes at 16 weeks of age, respectively.
004673	NOD.129(B6)-Rag1^tm1Mom Cd80^tm1Shr/JbsJ	Cryopreserved - Ready for recovery
	The NOD.129(B6)Rag1^tm1MomCd80^tm1Shr/JbsJ homozygous mice fail to produce T or B cells. Mice homozygous for both Rag1^tm1Mom and Cd80^tm1Shr are viable and fertile and exhibit no signs of diabetes due to the absence of lymphocytes. On the NOD background Cd80^tm1Shr alone exacerbates diabetes onset when compared to standard NOD controls. When injected with proteolipid protein in Complete Freund's Adjuvant, NOD mice homozygous for the Cd80^tm1Shr/JbsJ mutation alone develop similar though slightly milder, experimental autoimmune encephalomyelitis (EAE) when compared with NOD controls. NOD.129(B6)-Rag1^tm1MomCd80^tm1Shr/JbsJ are valuable for unraveling the co-stimulatory pathways of T cell activation as it relates to autoimmune diseases and organ transplantation.
005878	NOD.129(Cg)-Cd44^tm1Hbg/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected. Although lymphocyte development appears unremarkable, irregularities are observed in lymphocyte trafficking. Tail-injected lymphocytes derived from null animals exhibit an impaired ability to traffic to peripheral lymph nodes, and to a much greater degree, the thymus. Transcription and translation of the targeted allele subsequently lead to the synthesis of the lacZ protein under control of the 5' regulatory elements of the endogenous locus in all cells and tissues normally expressing one or several of the CD44 isoforms. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary f ..... For more information please see the full phenotype on the strain data sheet
002573	NOD.129P2(B6)-Il2^tm1Hor/DvsJ	Cryopreserved - Ready for recovery
	Heterozygotes and homozygotes have accelerated diabetes onset, compared with NOD controls, with homozygotes dying by 5 to 7 weeks of age and heterozygotes having an average lifespan of approximately 100 days. Treatment with complete Freund?s adjuvant can delay disease onset and extend lifespan to permit homozygotes to reproduce.
004222	NOD.129P2(B6)-Il4^tm1Cgn/DvsJ	Cryopreserved - Ready for recovery
	Complete Freund's adjuvant (CFA) induced suppression of diabetes in NOD mice has been associated with a shift to Th2 cytokine production. NOD mice deficient in IL4 were created to investigate the role of IL4 in this shift. Mice homozygous for the Il4^tm1Cgn targeted mutation are viable and fertile. T and B cell development is normal but IgG1and IgE levels and the ability of homozygous mutant mice to produce Th2-derived cytokines are significantly reduced. IL4 deficient NOD mice develop IDDM with the same incidence as standard NOD/Lt controls, and there is no change between IL4 deficient and wildtype NOD in disease protection conferred by treatment of bacillus Calmette-Guerin vaccine (BCG) or CFA. Both IL4 deficient and wildtype NOD mice are significantly protected from insulitis by treatment of CFA but not by treatment of BCG. (Serreze et al 2001)
004444	NOD.129P2(C)-Tcra^tm1Mjo/DoiJ	Cryopreserved - Ready for recovery
	NOD mice homozygous for the Tcra^tm1Mjo targeted mutation lack alpha beta T cells, and therefore, are completely protected from diabetes development. Because of the complete elimination of alpha beta T cells, these mice are useful in adoptive transfer experiments (as in Hoglund et al. 1999).
002575	NOD.129S7(B6)-Ifng^tm1Ts/DvsJ	Cryopreserved - Ready for recovery
	Mice homozygous for the Ifng^tm1Ts targeted mutation are viable and fertile. This Ifng -deficient mutant develops type 1 diabetes at the same rate as the NOD/ShiLt parental strain.
006775	NOD.Cg-Foxp3^sf/DoiJ	Cryopreserved - Ready for recovery
	Scurfy mice develop an X-linked lymphoproliferative disease resulting from defective T cell tolerance. By 3 weeks of age, Foxp3-deficient NOD mice suffer massive lymphoproliferation and inflammatory infiltration in lungs, liver, skin, pancreas, kidneys, stomach, colon, fat and muscles and die by three weeks of age. At 14 days of age, NOD.Foxp3-deficient mice developed exocrine pancreatitis and occasional peri-insulitis; however invasive insulitis and diabetes were not observed. In a NOD.Foxp3-deficient, BDC2.5 TCR transgenic model, mice experienced markedly decreased lymphoproliferation, yet 100% were diabetic by 20 days of age. This congenic NOD scurfy model is useful to study the role of Foxp3-dependent regulatory T cells on diabetes development.
005346	NOD.Cg-Il10^tm1Cgn Casp1^tm1Sesh/LtJ	Cryopreserved - Ready for recovery
	Mice homozygous for the Il10 and Casp1 targeted mutations are viable and fertile when housed under SPF conditions. NOD/Lt mice deficient for both of these genes develop type 1 diabetes at a rate equivalent to the parental strains. The Il10 targeted mutation also renders this NOD/Lt stock susceptible to colitis (although not as severe as other strains of Il10 deficient mice) when maintained under standard housing conditions.
004291	NOD.Cg-Il10^tm1Cgn Il4^tm1Cgn/DvsJ	Cryopreserved - Ready for recovery
	Mice homozygous for the Il10 and Il4 targeted mutations are viable and fertile when housed under SPF conditions. NOD/Lt mice deficient for both of these genes develop type 1 diabetes at a rate equivalent to the parental strain. The Il10 ^tm1Cgn mutation also renders this NOD/Lt stock susceptible to colitis (although not as severe as other strains of Il10 deficient mice) when maintained under standard housing conditions.
004266	NOD.Cg-Il10^tm1Cgn/DvsJ	Cryopreserved - Ready for recovery
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under SPF conditions. This mutant develops type 1 diabetes at the same rate as the NOD/Lt parental strain. The Il10 ^tm1Cgn mutation also renders this NOD/Lt stock susceptible to colitis (although not as severe as other strains of Il10 deficient mice) when maintained under standard housing conditions.
004347	NOD.Cg-Rag1^tm1Mom Tg(TcraAI4)1Dvs/DvsJ	Cryopreserved - Ready for recovery
	The rearranged Tcra transgene expressed in these mice is derived from the pancreatic beta cell-reactive CD8 T lymphocyte clone AI4. The presence of the nonfunctional Rag1^tm1Mom allele renders mice incapable of rearranging endogenous T cell receptor genes. When crossed with strain NOD.Cg-Tg(TcrbAI4)1DvsRag1^tm1Mom/DvsJ (004348), the resulting animals that carry both the alpha and beta AI4 TCR transgenes exhibit an accelerated development of insulin-dependent diabetes mellitus (IDDM). Additionally, transgenic animals bearing both TCR transgenes offer a source of CTL precursors useful in examining the diversity of beta cell peptides recognized by the autoreactive CD8+ T lymphocytes contributing to the earliest phase of IDDM development. Homozygous mice are viable and fertile.
006024	NOD.Cg-Rag1^tm1Mom H2-Ab1^tm1Gru Tg(CD4,HLA-DQA1,HLA-DQB1)N8Ell/EllJ	Cryopreserved - Ready for recovery
	Rag1 and H2-Ab1 deficient NOD mice carrying transgenes encoding humanized CD4 and HLA-DQ6 lack T and B cells and are free of autoimmune diabetes and cardiomyopathy, and do not develop thyroiditis. This model is useful in adoptive transfer experiments and in studying MHC class II-based resistance and susceptibility in autoimmunity.
006022	NOD.Cg-Rag1^tm1Mom H2-Ab1^tm1Gru Tg(CD2-CD4,HLA-DQA1,HLA-DQB1)1Ell/EllJ	Cryopreserved - Ready for recovery
	Rag1 and H2-Ab1 deficient NOD mice carrying transgenes coding for human CD2-CD4 and HLA-DQ8 lack T and B cells, and are diabetes free. Also, unlike the H2-Ab1 deficient, transgenic CD4, HLA-DQ8 mice (see Stock No. 006021), this strain does not develop cardiomyopathy. This model is useful in adoptive transfer experiments and to understand the role of MHC class II in autoimmunity.
005686	NOD.Cg-Thy1^a Tg(TcraCl4,TcrbCl4)1Shrm/ShrmJ	Cryopreserved - Ready for recovery
	Transgenic mice, commonly referred to as NOD.clone-4 TCR, are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities. The TCR expressed from this transgene is specific for influenza virus A/PR/8 hemagglutinin (HA) in the context of the MHC class I molecule H2-K^d. FACS analysis of pancreatic lymph node indicates CFSE treated NOD clone-4 T cells adoptively transferred into NOD.InsHA (Stock No. 005685) proliferate vigorously and there is a 2-3-fold increase in the percentage of dividing clone-4 TCR, CD8⁺ T cells when compared to BALB/cBy (Stock Nos. 005307 and 005533) or B10.D2 (Stock Nos. 005308 and 005534). HA specific reactivity not tolerance is observed. This mouse is further modified with the Thy1^a allele, rather than the alternate allele Thy1^b present in C57BL/10, DBA/2, BALB/c and NOD/Lt mice. Thus, cell populations derived from these transgenic mice c ..... For more information please see the full phenotype on the strain data sheet
000269	SB/LeJ	Cryopreserved - Ready for recovery
	The SB/Le inbred strain is homozygous for both the satin (Foxq1^sa) and beige (Lyst^bg) mutations. Most of the immunological phenotype is due to the beige mutation. Homozygous mutant beige mice are characterized by a condition that closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. They have a severe deficiency of natural killer (NK) cells. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibo ..... For more information please see the full phenotype on the strain data sheet
010968	SB;C3Sn-Lrp4^mdig-2J/GrsrJ	Cryopreserved - Ready for recovery
	Mice homozygous for the Lrp4^mdig-2J mutation have toes missing from each foot, have a coarse tail, and some, but not all, have one or two extra upper incisors.
003899	STOCK Cd44^tm1Hbg/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected. Although lymphocyte development appears unremarkable, irregularities are observed in lymphocyte trafficking. Tail-injected lymphocytes derived from null animals exhibit an impaired ability to traffic to peripheral lymph nodes, and to a much greater degree, the thymus. Transcription and translation of the targeted allele subsequently lead to the synthesis of the lacZ protein under control of the 5' regulatory elements of the endogenous locus in all cells and tissues normally expressing one or several of the CD44 isoforms.
005707	STOCK Rag1^tm1Mom Tg(TIE2-lacZ)182Sato/J	Cryopreserved - Ready for recovery
	Mice homozygous for both the targeted mutation and the transgene are viable and fertile. The transgene beta-galactosidase is well expressed, reflects endogenous Tek/Tie2 activity, and is specific to the vascular endothelium. Mice homozygous for the Rag1 mutation are immunodeficient as they lack mature B and T lymphocytes. This double mutant mouse may be useful in studies of cancer, tumor-related angiogenesis, and as a recipient of xenografted tumors.
002506	STOCK Tg(CD3E)26Cpt-Rag1^tm1Mom/J	Cryopreserved - Ready for recovery
	Mice carrying both the (CD3E)26Cpt transgene (Stock No. 002194) and the Rag1^tm1Mom targeted mutation exhibits characteristics of both mutant strains. Double homozygous mutant mice produce no mature T, B, or NK cells. They have no CD3⁺ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice contains 15 to 130 times fewer cells than heterozygous or wildtype siblings. The thymocytes are CD8^-CD4^- and most are IL2 receptor positive. Neither the spleen nor bone marrow contain any IgM or IgD staining cells, indicating an absence of mature B cells. These and other data suggest that B cell and T cell development has been arrested at an early stage.
013115	B6.Cg-Rag1^tm1Mom Tg(UBC-GFP)30Scha/J	Research Strain
	Tg(UBC-GFP)30Scha generates green fluorescent protein (GFP) expression in all cells of the body with cell lineage-specific variation in expression level. Hematopoetic cells have high expression levels compared with other cells and T cells have a 2-fold higher GFP expression level than that in CD19⁺B220⁺ B cells. The Rag1^tm1Mom targeted disruption, which blocks the intragenic recombination essential for T and B cell antigen receptor formation, leaves homozygous mice immunocompromised due to the inability to form functional, mature T and B cells. This strain, which combines this targeted mutation with this transgene, is a universal host that does not reject engraftment regardless of histoincompatibility and permits detection of host-derived embryos or tissues by detection of GFP, as long as the donor tissue is not also engineered to express GFP. Animals from this strain can also be used as sentinel mice in specific pathogen free environments. ..... For more information please see the full phenotype on the strain data sheet
002574	NOD.129P2(B6)-Il4^tm1Cgn/Dvs	Research Strain

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Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.
View a Data sheet for New Strains Awaiting Transfer
Select the strain name to link to the strain data sheet.

Stock Number	Strain Name Strain Description	Standard Supply
018055	B6.FVB-Tg(H2-K-S100a9,GFP)1Gabr/J	Awaiting Transfer from the Donor
These transgenic mice express S100a9 (S100 calcium binding protein A9 (calgranulin B)), a myeloid-related protein, and GFP under the control of the hematopoietic cell-specific H2-K promoter. Overexpression of S100a9 inhibits the differentiation of dendritic cells and macrophages while inducing an accumulation of myeloid-derived suppressor cells.

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New Strains Awaiting Transfer from the Donor
Receive periodic updates on the status of the colony AWAITING TRANSFER

Obtain advance notification of strain availability and opportunity to order prior to the strain being published as available

Provide input affecting speed and quantity of availability
The Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion.
It is VERY IMPORTANT that you register interest in strains Awaiting Transfer. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain. Registering interest also provides benefits to you (including advance notification of pending availability). Whether a strain is made available from a live colony OR from our cryopreservation repository, you may want to consider the option of Dedicated Supply. To learn more about Dedicated Supply, go to Services.

Additional Register Interest Strains

Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.
View a Data sheet for a Strain
Select the strain name to link to the strain data sheet.

Stock Number	Strain Name Strain Description	Standard Supply
009079	STOCK Mll1^{tm2(MLLT3)Thr}/KsyJ	On Hold
Beginning around six months of age, these Mll-AF9 knock-in mice recapitulate the acute myeloid leukemia (AML) phenotype associated with the t(9;11)(p22;q23) translocation in humans and may be useful for studying hematopoietic development, cancer, and acute myeloid leukemia.

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It is VERY IMPORTANT that you Register Interest. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain.

Send questions to our Technical Support team using the Express Technical Support Form.
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JAX® Mice Strains

New Strains Awaiting Transfer from the Donor

Additional Register Interest Strains

JAX^® Mice Strains