JAX Mice Database - Growth Factors/Receptors/Cytokines

Search Criteria: Research Area is "Immunology and Inflammation Research: Growth Factors/Receptors/Cytokines"

Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development

JAX^® Mice Strains

Stock Number	Strain Name Strain Description	Standard Supply
002287	B6.129S7-Ifng^tm1Ts/J	Level 2
	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.
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 descriiption 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.
004326	C3Bir.129P2(B6)-Il10^tm1Cgn/Lt	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 descriiption on the strain data sheet
005557	NOD.Cg-Prkdc^scid Il2rg^tm1Wjl/SzJ	Level 3
	The NOD.Cg-Prkdc^scid Il2rg^tm1Wjl/SzJ mice, commonly known as NOD scid gamma (NSG), do not express the Prkdc gene nor the X-linked Il2rg gene. NSG mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Histological examination of lymphoid tissues reveals absence of lymphoid cells and some cystic structures in the thymus, an absence of follicles in the spleen and markedly diminished celluarity of lymph nodes. NSG mice are deficient in mature lymphocytes, serum Ig is not detectable and natural killer (NK) cell cytotoxic activity is extremely low. These mice are resistant to lymphoma development even after sublethal irradiation treatment. These mutant mice have been shown to readily support engraftment of human CD34⁺ hematopoietic stem cells and represent a superior, long-lived model suitable for studies employing xenotransplantation strategies. Please note that the NSG carries the tr ..... For more information please see the full descriiption on the strain data sheet
002818	B6.129-Tnfrsf1a^tm1Mak/J	Level 4
	Mice homozygous for the Tnfrsf1a^tm1Mak targeted mutation (formerly Tnfr1^tm1Mak) have normal thymocyte development, lymphocyte populations and clonal deletion of potentially self-reactive T cells. TNF signaling is largely abolished, with no TNF induction of NF-kB. Homozygous mutant mice are resistant to lethal dosages of either lipopolysaccharides or S. aureus enterotoxin but succumb to L. monocytogenes infection. TNFRSF1an may also protect against atherosclerotic lesion development in mice fed an atherogenic diet.
002693	B6.129S1-Il12b^tm1Jm/J	Level 4
	Mice homozygous for the Il12b^tm1Jmtargeted mutation have a severely restricted ability to mount a TH1 response to in vivo endotoxin administration as evidenced by decreased interferon-gamma production although IL2 (IL-2) production is not compromised. The TH2 response is enhanced as evidenced by increased secretion of IL4 (IL-4). Delayed type hypersensitivity (DTH) responses are reduced. Also see the Il12a-deficient strains (Stock No. 002691 & 002692).
003288	B6.129S7-Ifngr1^tm1Agt/J	Level 4
	Mice homozygous for the Ifngr1^tm1 targeted mutation are viable and fertile with no overt abnormalities. They have normal T cell responses but are defective in natural resistance, evidenced by an increased susceptibility to infection by Listeria monocytogenes and vaccinia virus.
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 descriiption on the strain data sheet
003243	B6;129S-Tnfrsf1a^tm1Imx Tnfrsf1b^tm1Imx/J	Level 4
	Mice homozygous for both the Tnfrsf1a^tm1Imx and Tnfrsf1b^tm1Imx targeted mutations (p55 and p75 deficient) are viable and fertile. Double homozygous mutant mice fail to bind TNF. Thymus, spleen, and other lymphoid tissue are normal, indicating that TNF is not required for normal development of these organs.
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.
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 descriiption on the strain data sheet
002702	129-Ifngr1^tm1Agt/J	Repository- Live
	Mice homozygous for the Ifngr1^tm1Agt targeted mutation are viable and fertile with no overt abnormalities. They have normal T cell responses but are defective in natural resistance, evidenced by an increased susceptibility to infection by Listeria monocytogenes; and vaccinia virus.
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 descriiption on the strain data sheet
006102	B10.Cg-H2^k Tg(Il2/NFAT-luc)83Rinc/J	Repository- Live
	Hemizygous transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. The donating investigator reports that homozygous females in their colony are subfertile. These transgenic mice express luciferase under the regulation of the Il2 minimal promoter and 3 binding sites for the NFAT inducible nuclear factor involved in the regulation of interleukin-2 and other cytokine expression. Luciferase activity in these transgenic mice identifies NFAT-mediated transcription. These NFAT-luc transgenic mice may be useful be useful as reporters for NFAT-mediated expression during thymocyte development and selection and in studies related to signal transduction, apoptosis, and transcriptional regulation.
006412	B6.129-Il12b^tm1Lky/J	Repository- Live
	Mice homozygous for this bicistronic "yet40" allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The IRES-EYFP is inserted downstream of the endogenous stop codon, allowing for normal expression of the endogenous gene and simultaneous EYFP reporter expression. ELISA assays confirm that p40 protein is expressed at similar levels in homozygous mutant and wildtype mice. The EYFP reporter marks dendritic cell (DC) and macrophage lineage cells that produce p40 following stimulation with toll-like receptor (TLR) ligands both in vivo and in vitro. These mice may be useful for labeling activated IL12/23 p40 expressing cells in studies of immunology and immunity, TLR signal cascades, cancer immunity, and vaccine development.
008451	B6.129P(Cg)-Ptprc^a Cx3cr1^tm1Litt/LittJ	Repository- Live
	Mice that are homozygous for the CX3CR1-GFP targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. RT-PCR analysis of lymphoid tissue from homozygotes detects mutant gene product (mRNA) and no wild type gene product (mRNA). Flow cytometric analysis of peripheral blood cells identified a subset of green fluorescent cells not observed in wild type mice. Enhanced Green Fluorescent Protein (EGFP), but not the endogenous gene, is expressed in monocytes, dendritic cells, NK cells, and brain microglia, mimicking endogenous gene expression. The same subset of peripheral blood cells isolated from heterozygote mice express detectable levels of EGFP. Immunohistochemical analysis of spleen and peripheral nerve tissue from homozygotes does not detect EGFP. These mice also express the CD45.1 (Ly5.1 or Ptprc^a) allele, which is atypical for the C57BL/6 congenic background, and this marker may be used to track donor cell popul ..... For more information please see the full descriiption on the strain data sheet
005582	B6.129P-Cx3cr1^tm1Litt/J	Repository- Live
	Mice that are homozygous for the CX3CR1-GFP targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. RT-PCR analysis of lymphoid tissue from homozygotes detects mutant gene product (mRNA) and no wild type gene product (mRNA). Flow cytometric analysis of peripheral blood cells identified a subset of green fluorescent cells not observed in wild type mice. Enhanced Green Fluorescent Protein (EGFP), but not the endogenous gene, is expressed in monocytes, dendritic cells, NK cells, and brain microglia, mimicking endogenous gene expression. The same subset of peripheral blood cells isolated from heterozygote mice express detectable levels of EGFP. Immunohistochemical analysis of spleen and peripheral nerve tissue from homozygotes does not detect EGFP. These CX3CR1-GFP mutant mice may be useful in studies of leukocyte migration and trafficking, as well as for transplantation studies. Of note, CX3CR1-GFP mice are also avail ..... For more information please see the full descriiption on the strain data sheet
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 descriiption on the strain data sheet
007572	B6.129P2(Cg)-Rorc^tm2Litt/J	Repository- Live
	Mice homozygous for this Rorc(γt^GFP (or RORγt)^GFP) mutant allele are viable and fertile. While Rorcγ mRNA is detected in liver in Rorc(γ)t^GFP homozygotes, mRNA and protein for the thymus-specific isoform (Rorcγt) encoded by the targeted allele are not detected in the thymus. EGFP expression reports Rorc(γt) transcription in the thymi of adult Rorc(γt)GFP mice. Homozygous mice exhibit abnormal lymph node, Peyer's patch, and lymphoid tissue inducer (LTi) cell development. Mice with Rorcγt-deficient T cells lack tissue-infiltrating proinflammatory T-helper cells (Th17 cells), and are protected from induced autoimmune disease (EAE) on this genetic background. The donating investigator also reports increased thymoma incidence with age in homozygotes. These RorcγtGFP mutant mice may be useful in studying immune system homeostasis, T cell repertoire selection, CD4/CD8 double positive (CD4⁺/CD8 ..... For more information please see the full descriiption on the strain data sheet
002687	B6.129P2-Ccl3^tm1Unc/J	Repository- Live
	Mice homozygous for the Scya3^tm1Unc targeted mutation are viable and fertile. Homozygous mutant mice are resistant to Coxsakievirus-induced myocarditis. Mutant mice infected with influenza virus show reduced pneumonitis and delayed clearance of virus. There are no overt hematopoietic abnormalities. Also known as macrophage inflammatory protein 1a, Mip1a.
005427	B6.129P2-Ccr5^tm1Kuz/J	Repository- Live
	At birth, mice homozygous for the targeted allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No transcript is detected in splenocytes or peritoneal macrophages. Thioglycollate-elicited peritoneal macrophages from homozygotes exhibit a delayed period before reaching peak mobilization (72 hours vs. 36 for wild type mice). 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 5427. 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.
002928	B6.129P2-Cd40^tm1Kik/J	Repository- Live
	Mice homozygous for the targeted mutation are viable and fertile. Homozygous mutant mice exhibit impaired immunoglobulin class switching and germinal center formation.
004130	B6.129P2-Il18^tm1Aki/J	Repository- Live
	Mice that are homozygous null for the Il18 gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Il18 gene product (mRNA or protein) is detected. Homozygous null mice exhibit reduced levels of interferon gamma in response to heat killed bacteria and lipopolysaccharide. IL-12 levels in the serum are similar to wild type after LPS challenge, indicating that the decreased interferon gamma response in Il18 deficient mice is not due to low induction of IL-12. Il18 deficient mice also exhibit diminished natural killer cell activity and impaired T helper lymphocyte response.
004131	B6.129P2-Il18r1^tm1Aki/J	Repository- Live
	Mice that are homozygous null for the Il18r1 gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Il18r1 mRNA is detected. Homozygous Il18r1 null mice are similar in phenotype to IL-18-deficient mice. They show reduced binding of IL-18 on the surface of Th1 cells, and exhibit decreased levels of interferon gamma production in response to IL-18. Natural killer cell activity is also diminished and the T helper lymphocyte response in impaired.
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 descriiption on the strain data sheet
002253	B6.129P2-Il4^tm1Cgn/J	Repository- Live
	Mice homozygous for the Il4^tm1Cgn targeted mutation are viable and fertile. T and B cell development is normal but IgGl and IgE levels and the ability of homozygous mutant mice to produce Th2-derived cytokines are significantly reduced.
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.
005576	B6.129P2-P2rx7^tm1Gab/J	Repository- Live
	Mice that are homozygous for the targeted allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected in cultured bone marrow mast cells or peritoneal macrophages. Samples of whole blood, as well as peritoneal macrophages, derived from mutant mice fail to produce extracellular interleukin 1 beta in response to lipopolysaccharide (LPS) and ATP treatment. Similarly, peritoneal lavage fluids from mutant animals that have been primed with LPS and subsequently challenged with ATP, are deficient in mature interleukin 1 beta, and at later time points, exhibit attenuated interleukin 6 levels when compared to fluids from similarly treated wildtype mice. Peripheral blood monocytes and leukocytes fail to change shape/volume and shed L-selectin in response to ATP. Mutant mice exhibit reduced induction and severity of monoclonal anti-collagen-induced arthritis. Mutant mice also display significant reduct ..... For more information please see the full descriiption on the strain data sheet
004754	B6.129S-Il1rn^tm1Dih/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable and do not display any gross physical or behavioral abnormalities. By 6 weeks of age homozygous mice have lower body weight. Homozygous females may have reduced litter sizes. No gene product (mRNA) is detected by Northern blot analysis of lung tissue after lipopolysaccharide (LPS) challenge. Mice homozygous for the mutation are less susceptible to experimental Listeria monocytogenes infection, but are more susceptible to LPS endotoxin challenge. After LPS challenge IL-1 levels are decreased. Basal serum amyloid protein and serum IL-6 levels are higher. Hepatic acute phase protein inflammatory response and mortality to subcutaneous turpentine abscess induction are increased. When fed a high fat diet containing cholate for 12 weeks, homozygotes exhibit a 3-fold decrease in total cholesterol (non-HDL). Heterozygotes fed the same diet exhibit an intermediate decrease in total cholesterol. Immunohistochemical analysis of h ..... For more information please see the full descriiption 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 descriiption on the strain data sheet
005940	B6.129S1-Csf2rb^tm1Cgb/J	Repository- Live
	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 descriiption on the strain data sheet
002692	B6.129S1-Il12a^tm1Jm/J	Repository- Live
	Mice homozygous for the Il12a^tm1Jm targeted mutation on a normally resistant 129/Sv genetic background are unable to restrict the progression of Leishmania major infection, demonstrating the importance of this cytokine for developing such resistance. Homozygotes are unable to mount a delayed-type hypersensitivity (DTH) reaction but a TH2 response is induced. Also known as p35. Please refer to the Il12b-deficient related targeted mutations (Stock No. 002693 and 002694). 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 a ..... For more information please see the full descriiption on the strain data sheet
003248	B6.129S1-Il12rb2^tm1Jm/J	Repository- Live
	Mice homozygous for the Il12rb2^tm1Jm targeted mutation are viable and fertile. Homozygous mutant mice do not show an increased susceptibility to infections. 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.
006416	B6.129S1-Map2k3^tm1Flv/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. However, the donating investigator reports that reproductive performance is poor for unknown reasons. No gene product (mRNA or protein) is detected by Northern blot analysis of liver and kidney or Western blot analysis of peritoneal macrophages. Mutant mice exhibit an impaired type I cytokine immune response with reduced induced interferon gamma production. Macrophages from mutant mice have a reduced p39 MAPK activation and IL-12 production when challenged with LPS lipopolysaccharide). Dendritic cells also have reduced IL-12 production response. Mutant mouse embryo fibroblasts (MEF) have a reduced cytokine expression response to tumor necrosis factor (TNF). This mutant mouse strain may be useful in studies of inflammatory response. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles ..... For more information please see the full descriiption on the strain data sheet
006848	B6.129S2(C)-Il8rb^tm1Mwm/J	Repository- Live
	The donating investigator reports that homozygous mice are viable and fertile but few pups are produced, and they need a gnotobiotic facility to thrive. Homozygous mice have several abnormalities, including neurological defects, impaired wound healing, impaired angiogenesis, and altered growth of induced/implanted tumors. Homozygotes may also exhibit splenomegaly, lymphadenopathy, and increased susceptibility to various pathogens due to impaired neutrophil recruitment and decreased pathogen clearance during innate immune responses. These mutant mice may be useful in studies of inflammation and immunology and cancer biology. 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 becom ..... For more information please see the full descriiption on the strain data sheet
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 descriiption on the strain data sheet
002258	B6.129S2-Lta^tm1Dch/J	Repository- Live
	Mice homozygous Lta^tm1Dch targeted mutation are viable and fertile. Homozygous mutant mice show abnormal development of peripheral lymphoid organs with no detectable popliteal, inguinal, para-aortic, mesenteric, axillary, or cervical lymph nodes, and no detectable Peyer's patches. Morphological changes in the spleen white pulp were accompanied by alterations in T and B cell content. CD4⁺ and CD8⁺ T cells counts in peripheral blood are normal but there is a four-fold increase in B cells. Neutrophil, monocyte, and platelet counts are normal. The thymus contains normal numbers of CD4⁺CD8⁺, CD4⁺, CD8⁺, and CD4^-CD8^- T cells. Splenic T cells develop normal MHC class I and class II-restricted allocytotoxic responses. Also known as tumor necrosis factor beta, Tnfb.
002620	B6.129S2-Tnfrsf1b^tm1Mwm/J	Repository- Live
	Mice homozygous for a Tnfrsf1b^tm1Mwm targeted mutation (formerly Tnfr2^tm1Mwm, p75 deficient) are viable and fertile. Homozygous mutant mice show normal T-cell development and activity, but are resistant to TNF-induced cell death. Subcutaneous injections of TNF into homozygotes elicit much less tissue necrosis.
008117	B6.129S4(129S6)-Sst^tm1Ute/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 by Northern blot, in situ hybridization or radioimmunoassay analysis of brain tissue. Homozygotes exhibit increased baseline plasma growth hormone, corticosterone and total ghrelin levels compared to wildtype. Mutant mice have impaired motor performance ability. Somatostatin-deficient mice have enlarged stomachs with an increased number of parietal cells and hyperchlorhydria. Hippocampal neprilysin activity is diminished. Compared to wildtype controls, amyloid beta 42 peptides levels are elevated in the hippocampus. This mutant mouse strain may be useful in studies of gastric homeostasis, learning and memory and endocrinology.
006087	B6.129S4-Cxcl10^tm1Adl/J	Repository- Live
	Homozygous mice are viable, fertile, and have no overt morphological or developmental abnormalities. No endogenous gene expression is observed in bone marrow-derived macrophages before or after IFN-gamma stimulation. Homozygous mice have defective T cell responses, including impaired proliferation and IFN-gamma secretion following antigenic challenge (129Sv background). In experimental models of T helper-1 (Th1)-mediated immune responses, homozygous-deletion leads to diminished immune function; contact hypersensitivity is reduced (129Sv background) and diminished threshold for disease expression in experimental autoimmune encephalomyelitis (EAE, human model of multiple sclerosis) (C57BL/6 background). After injection with a neurotropic coronavirus MHV, null mice (on a B6;129Sv background) exhibit impaired viral clearance, decreased CD4⁺/CD8⁺ infiltration into the brain, and are protected from viral-induced demyelination. Similarly, homozygous mice (on a C57BL/6 ba ..... For more information please see the full descriiption on the strain data sheet
002952	B6.129S4-Il2ra^tm1Dw/J	Repository- Live
	Mice homozygous for the Il2ra^tm1Dw targeted mutation are are characterized by a lymphoproliferative disorder, hemolytic anemia, and an inflammatory bowel disease beginning at approximately 9 weeks of age; also known as p55 gene chain, Ly43, CD25.
003174	B6.129S4-Il2rg^tm1Wjl/J	Repository- Live
	Mice homozygous for the Il2rg^tm1Wjl targeted mutation are viable and fertile. Mutant mice have hypoplastic thymuses with a 10-fold reduction in the absolute number of lymphocytes. They have a limited number of mature splenic B and T cells, lack NK cells and Peyer's patches, and development of gut-associated intraepithelial lymphocytes is diminished. In vitro studies show defects in NK activity, IL4-directed Ig class switching of thymocytes, and thymocyte mitogenic responses.
008076	B6.129S4-Traf1^tm1Tsi/J	Repository- Live
	Mice homozygous for the TRAF1 mutant allele (TRAF1^-/-) are viable and fertile. No protein expression from the targeted gene is observed in CD40-stimulated splenocytes isolated from homozygous mice. Homozygous mice on a C57BL/6 congenic background (B6-TRAF1^-/-) have abnormal memory T cell survival and impaired influenza virus CD8 T cell responses. Activated B6-TRAF1^-/- T cells accumulate increased levels of proapoptotic BH3-only family member Bim, particularly the most toxic isoform, Bim_s. The donating investigator reports that B6-TRAF1 mutant mice may be difficult to breed and gain more weight than BALB/c-TRAF1 mutant mice. Homozygous mice on a BALB/c congenic background (BALB/c-TRAF1^-/-) exhibit acute liver injury and elevated serum liver enzymes following intratracheal TNF-alpha treatment. Furthermore, activated TRAF1^-/- T cells have significantly increased expression of Th2 cytokines (IL-4, IL-5 and IL-13) that el ..... For more information please see the full descriiption on the strain data sheet
006133	B6.129S4-Vdr^tm1Mbd/J	Repository- Live
	Heterozygous mice are phenotypically indistinguishable from wildtype siblings. Homozygous mice are viable and fertile with normal survival until approximately 14 months. RNA isolated from the intestine and kidney show a truncated deletion of the second zinc finger coding region followed by a premature termination codon, resulting in the absence of receptor protein. Homozygous mice exhibit an identical phenotype as the human disease hereditary vitamin D-dependent rickets type II (HVDDR). As early as 21 days of age, mutant mice demonstrate hypocalcemia, hypophosphatemia, hyperparathyroidism, increased serum parathyroid hormone, abnormal blood mineral levels, and growth retardation. In addition, renin and plasma angiotensin II levels are increased. Homozygous mice are hypertensive and exhibit cardiachypertrophy. At 4 weeks of age, homozygous mice exhibit perioral and periorbital alopecia that progresses over the entire body by 4 months of age. Rickets and osteomalacia develop by 35 days. ..... For more information please see the full descriiption on the strain data sheet
003245	B6.129S7-Il1r1^tm1Imx/J	Repository- Live
	Mice homozygous for the Il1r^tm1Imx targeted mutation fail to respond to IL1. They display normal acute phase response to systemic LPS challenge, but have defective responses to local turpentine induced inflamation. Homozygotes display increased frequency and severity of S. aureus septic arthritis.
002295	B6.129S7-Il7r^tm1Imx/J	Repository- Live
	Mice homozygous for the Il7r^tm1Imx targeted mutation are viable and fertile. Newborn and young adult homozygous mutant mice have dramatically reduced thymic and splenic lymphoid cellularity in both B and T cell compartments. T cell development is affected prior to surface expression of CD4 and CD8 and prior to the initiation of T cell receptor beta chain rearrangement. B cell development is through pre-pro-B cells (Cd43⁺ HSA^dull). The phenotype in the mouse resembles human interleukin-2 receptor gamma deficiency (XSCID). IL2Rgamma has been shown to be a necessary component of the IL7R providing the biochemical basis for this condition.
006112	B6.129X1-Ela2^tm1Sds/J	Repository- Live
	Homozygous mice are viable, fertile and phenotypically normal in the absence of inflammatory stress. Homozygotes do not express the targeted gene in bone marrow myeloid cells. Homozygous mice have increased susceptibility to sepsis, morbidity, and mortality following intraperitoneal injection of Gram-negative (e.g. (K. pneumoniae and E. coli), but not Gram-positive (e.g. (S. aureus), bacteria. Despite this, mutant mice are not at increased risk to spontaneous infection. Although neutrophil, T cell, and macrophage migration/recruitment to the site of infection is unaffected in homozygous mutant mice, neutrophils show impaired bactericidal activity. Further, homozygous mice treated with a broad-spectrum inflammatory stimulus (zymosan) have impaired leukocyte firm adhesion and transmigration as well as reduced pro-inflammatory cytokine production. Upon exposure to cigarette smoke, homozygous mice are protected from the accumulation of neutrophils and macrophages in th ..... For more information please see the full descriiption 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.
007745	B6.Cg-Mirn155^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 descriiption on the strain data sheet
004201	B6.Cg-Selplg^tm1Fur/J	Repository- Live
	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.
004103	B6.Cg-Tac1^tm1Bbm/J	Repository- Live
	Mice that are homozygous null for the Tac1 gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Tac1 protein products (substance P or neurokinin A) are not immunodetectable. These mice have significantly reduced nociceptive pain responses to moderate to intense stimuli. Neurogenic inflammation is absent. Mutant mice are resistant to kainate-induced seizures and neurotoxicity. These mice provide a useful tool for studying the contribution of tachykinin peptides to pain processing and inflammatory disease states.
006098	B6.Cg-Tg(Il2/NFAT-luc)83Rinc/J	Repository- Live
	Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Homozygous females are subfertile. These transgenic mice express luciferase under the regulation of the Il2 minimal promoter and 3 binding sites for NFAT, an inducible nuclear factor involved in the regulation of interleukin-2 and other cytokine expression. Luciferase activity in these transgenic mice identifies NFAT-mediated transcription. These mice may be useful as reporters for NFAT-mediated expression during thymocyte development and selection and in studies related to signal transduction, apoptosis, and transcriptional regulation.
000160	B6.D2-Kitl^Sl-d/J	Repository- Live
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, steel-Dickie homozygotes (Kitl^Sl-d/Kitl^Sl-d) and compounds of steel and steel Dickie (Kitl^Sl/Kitl^Sl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel Dickie and steel heterozygotes. Mast cells are virtually absent in skin and other tissu ..... For more information please see the full descriiption on the strain data sheet
002782	B6;129P2-Ccr5^tm1Kuz/J	Repository- Live
	At birth, mice homozygous for the targeted allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No transcript is detected in splenocytes or peritoneal macrophages. Thioglycollate-elicited peritoneal macrophages from homozygotes exhibit a delayed period before reaching peak mobilization (72 hours vs. 36 for wild type mice).
003244	B6;129S-Tnfrsf1a^tm1Imx Il1r1^tm1Imx/J	Repository- Live
	Mice homozygous for both targeted mutations (called TNFRp55(-/-)-IL-1RI(-/-), TNFR1/IL1R1 or IL-1R1/TNFR1 KO) are viable and fertile, lacking both interlekin-1 beta type 1 receptor (IL1R1) and tumor necrosis factor alpha p55 (type 1) receptor (TNFR1). Double homozygotes exhibit characteristics of both the single "knockouts" including reduced inflammatory responses, reduced delayed-type hypersensitivity response, and remain highly susceptible to infection by Listeria monocytogenes. Homozygous mutant mice also have defects in Peyer's patch development, splenic architecture, formation of germinal centers and liver regeneration. Furthermore, IL-1R1/TNFR1 KO mice exhibit alterations in rapid eye movement sleep (REMS) and non-rapid eye movement sleep (NREMS) (a sleep phenotype different from that observed for mice singly homozygous for one or the other of these cytokine receptors), as well as differences in NREMS and REMS following sleep deprivation compared to control mice.
003018	B6;129S1-Il1r1^tm1Roml/J	Repository- Live
	Mice homozygous for the Il1r1^tm1Roml targeted mutation exhibit a reduced inflammatory response and no response to interleukin-1 alpha or beta. IL1 receptor type I deficient mice have a reduced delayed type hypersensitivity response and are highly susceptible to infection by Listeria monocytogenes.
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).
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.
000231	B6C3Fe a/a-Csf1^op/J	Repository- Live
	Mice homozygous for the osteopetrosis spontaneous mutation (Csf1^op) are viable and exhibit osteopetrosis. The osteoclasts are the primary cell type affected in homozygous mutant mice. This results in a generalized macrophage deficiency, monocytopenia, and defective bone remodeling. Homozygous mutant mice also have abnormal calcium regulation, impaired dental growth and female mice fail to lactate. Total leukocyte counts are reduced and marrow cells are decreased to one-tenth of normal control mice. Homozygous mutant mice have a deficient microglia and macrophage response, and therefore may be useful tools to study the role of glia in neurological disease if mated to transgenic models of neurodegenerative disease.
002496	BALB/c-Il4^tm2Nnt/J	Repository- Live
	Mice homozygous for the Il4^tm2Nnt targeted mutation are viable and fertile. T and B cell development is normal but IgGl and IgE levels and the ability of homozygous mutant mice to produce Th2-derived cytokines are significantly reduced. Susceptible to infection by Leishmania major despite deficiency in IL4.
003514	BALB/c-Il4ra^tm1Sz/J	Repository- Live
	Mice homozygous for the Il4ra ^tm1Sz targeted mutation are viable and fertile. While homozygous mutant mice show no overt phenotypic abnormalities they do exhibit a loss of Il4 signal transduction. This lack of response to Il4 results in a diminished TH2 helper T cell response to helminthic parasite infections. Il4ra-deficient mice provide a tool for analyzing the physiological pathways through which priming for TH2 responses are induced and the role of Il4 in a wide variety of infectious and other pathological conditions.
004190	C.129-Il4^tm1Lky/J	Repository- Live
	Mice homozygous for the targeted allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. A knockin replaces the endogenous gene with an Il4/IRES/EGFP gene (IL4 activity remains intact). This leads to generation of a bicistronic transcript under the control of endogenous regulatory elements. Cells activated to express IL4 will express EGFP, allowing reliable in vivo tracking of both innate and adaptive immune cells, and/or enabling their isolation without further stimulation. As the IRES element promotes translational competence capable of revealing low-level transcription otherwise not apparent from the canonical 5'-cap of the mRNA, cells from these mice can also be used to report competence for IL4 production upon stimulation.
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 descriiption on the strain data sheet
002691	C.129S1(B6)-Il12a^tm1Jm/J	Repository- Live
	Mice homozygous for the Il12a^tm1Jm targeted mutation on a normally resistant 129/Sv genetic background are unable to restrict the progression of Leishmania major infection, demonstrating the importance of this cytokine for developing such resistance. Homozygotes are unable to mount a delayed-type hypersensitivity (DTH) reaction but a TH2 response is induced. Also known as p35. Please refer to the Il12b-deficient related targeted mutations (002693 & 002694). 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.
002694	C.129S1-Il12b^tm1Jm/J	Repository- Live
	Mice homozygous for the Il12b^tm1Jm targeted mutation have a severely restricted ability to mount a TH1 response to in vivo endotoxin administration as evidenced by decreased interferon-gamma production although IL2 (IL-2) production is not compromised. The TH2 response is enhanced as evidenced by increased secretion of IL4 (IL-4). Delayed type hypersensitivity (DTH) responses are reduced. Also see the Il12a-deficient strains (002691 & 002692).
002724	C.129S2(B6)-Il8rb^tm1Mwm/J	Repository- Live
	Mice homozygous for the Il8rb^tm1Mwm targeted mutation are viable and fertile although the reproductive rate is lower than normal wildtype siblings. Homozygous mutant mice have splenomegaly, lymphadenopathy, and impaired neutrophil migration. Formerly referred to as Cmkar2, chemokine (C-X-C) receptor 2; also called Il8r, interleukin 8 receptor.
007680	C.129X1-Il4ra^tm1Tch/J	Repository- Live
	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 descriiption on the strain data sheet
002518	C57BL/6-Il4^tm1Nnt/J	Repository- Live
	Mice homozygous for the Il4^tm1Nnt targeted mutation are viable and fertile. T and B cell development is normal but IgGl and IgE levels and the ability of homozygous mutant mice to produce Th2-derived cytokines are significantly reduced.
002965	C57BL/6-Itgb7^tm1Cgn/J	Repository- Live
	Mice homozygous for the Itgb7^tm1Cgn targeted mutation have a marked hypoplasia of the gut-associated lymphoid tissue (GALT). This deficit is apparently due to the failure of Itgb7-deficient lymphocytes to arrest and adhere in the GALT.
008158	C57BL/6-Serpinb9^tm1Arp/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) is detected by RT-PCR analysis of myeloid and lymphoid cells. After experimental viral infection, homozygous mice have lower (five to nine-fold reduction) numbers of virus specific cytotoxic T lymphocytes (CTLs) and increased apoptosis of virus specific CD8 T cells when compared to wildtype controls. Mutant mice have impaired Lymphocytic Choriomeningitis virus (LCMV) infection clearance. Granzyme A and granzyme B specific activity is reduced in cytotoxic granules and increased in CTL cytoplasm. Mutant CTLs have a three-fold increase in the number of granules lacking granzyme B. This mutant mouse strain may be useful in studies of viral immune response and inflammation, and the exocytosis pathway in CTL apoptosis.
003242	C57BL/6-Tnfrsf1a^tm1Imx/J	Repository- Live
	Mice homozygous for the Tnfrsf1a^tm1Imx targeted mutation (formerly Tnfr1^tm1Imx, p55 deficient) show defects in resistance to intracellular pathogens and are resistant to the lethal effects of LPS administration in conjunction with D-galactosamine. Pulmonary inflammatory responses are diminished in p55 deficient mice. There are also defects in Peyer's patch development, splenic architecture, formation of germinal centers, and liver regeneration. TNFRSF1 deficient mice display increased susceptibility to atherosclerosis when maintained on a high fat diet.
007225	FVB.129(B6)-Usp18^tm1Dzh/J	Repository- Live
	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 descriiption on the strain data sheet
007799	NOD.Cg-Rag1^tm1Mom Il2rg^tm1Wjl/SzJ	Repository- Live
	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 descriiption on the strain data sheet
006956	NOD.Cg-Vdr^tm1Ska/CmatJ	Repository- Live
	Heterozygous mice are viable, fertile, and phenotypically indistinguishable from wildtype siblings. Homozygous mutant mice are viable but infertile. No VDR mRNA is detected by RT-PCR in samples from the intestine or kidney or from homozygous mutant embryo. Increased expression of CTP27B1 and reduced expression of CYP24A1 and calbindin-D9k is detected by RT-PCR in samples from VDR-deficient kidneys. Although mice homozygous for this targeted mutation are viable, shortly after weaning they exhibit dysmorphic features including a flat face and short nose, alopecia, growth retardation, and skeletal defects including hypocalcaemia, decreased bone mineral density, widened growth plates with hypomineralization, less trabeculae and thicker osteo seams. Homozygous mutant mice exhibit metabolic imbalances including abnormally high and low levels of 1,25(OH),2D3 and 25(OH)D3, respectively and abnormal cytokine and chemokine profiles. Homozygous mice exhibit normal pancreatic islet archite ..... For more information please see the full descriiption on the strain data sheet
000693	WC/ReJ Kitl^Sl/J	Repository- Live
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. Kitl^Sl/Kitl^Sl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing ..... For more information please see the full descriiption on the strain data sheet
100401	WCB6F1/J Kitl^Sl Kitl^Sl-d	Repository- Live
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Many steel alleles cause severe anemia resulting in death in utero of homozygous mutant mice. However, mice homozygous for some steel mutations and compound heterozygotes for two steel alleles (e.g., Kitl^Sl/Kitl^Sl-d) are viable and have black eyes and a white coat; they have severe macrocytic anemia, and both sexes are usually sterile due to failure of germ cells to migrate correctly during development. Mice heterozygous for a single steel mutation have diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtuall ..... For more information please see the full descriiption on the strain data sheet
002497	129-Ntf5^tm1Jae/J	Repository-Cryopreserved
	Mice homozygous for the targeted mutation are viable and fertile. Homozygous mutant mice lose sensory neurons in the nodose-petrosal and geniculate ganglia. However, they do not show loss of facial nucleus motor neurons, sympathetic neurons of the superior cervical ganglion, or dopaminergic neurons in the substantia nigra.
005320	129.Cg-Ppia^tm1Lubn/J	Repository-Cryopreserved
	Mice that are homozygous for the targeted mutation are viable, normal in size, and do not display any gross behavioral abnormalities. Homozygotes have reduced fertility. No gene product (protein) is detected by Western blot analysis. Approximately one third of homozygotes spontaneously develop blepharitis (inflammation of the eyelids). Histological examination reveals mononuclear cell, eosinophil and mast cell infiltration of the eyelid. Homozygotes exhibit splenomegaly and elevated levels of total serum IfG1 and IgE. CD4+ T cells isolated from homozygous mice have increased production of IL-2 (3 to 5 times normal) and IL-4. Cultured effector/memory CD4+ T cells are hypersensitive to TCR stimulation and have elevated Th2 cytokine production. This mutant mouse strain may be useful in studies of allergic reactions and effects of cyclosporine on signal transduction.
003117	129S-Sst^tm1Ute/J	Repository-Cryopreserved
	Mutant mice are healthy, fertile and of normal body size despite having three times the plasma growth hormone levels than wildtype littermates. Somatostatin is virtually absent in the adult cerebellum but is expressed during development. There is impaired motor learning and motor coordination as demonstrated in accelerating rotorod testing.
000090	129S1/Sv-Oca2⁺ Tyr⁺ Kitl^Sl-J/J	Repository-Cryopreserved
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. Kitl^Sl/Kitl^Sl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing a ..... For more information please see the full descriiption on the strain data sheet
000004	ABP/LeJ	Repository-Cryopreserved
	Mice homozygous for the Tgfa^wa1 spontaneous mutation are recognizable at 2 or 3 days of age by their curly whiskers. The first coat is strongly waved and straight in later coats. Most of the whiskers also become straight, but the guard hairs are curved and shorter than normal. Some homozygotes have eyelids open at birth. Mice homozygous for the recessive Adamts20^bt mutation have a dorsal and a ventral unpigmented patch posterior to the midline of the trunk with the dorsal patch usually being larger than the ventral patch. These patches run in a more transverse orientation across the mouse than lengthwise and often extend around the sides of the mouse to form a white belt. The size of the patches can vary from approximately 1 to 20 percent of the surface. Unlike other spotting mutations, no variability in phenotype was identified when belted was transferred onto the C57BL/6J or JU/CtLm backgrounds (Lamoreaux 1999). Murray and Snell reported findin ..... For more information please see the full descriiption on the strain data sheet
006100	B10.Cg-H2^k Tg(NFkB/Fos-luc)26Rinc/J	Repository-Cryopreserved
	Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Mutant mice have the luciferase gene driven by two copies of the NF-kappaB (NF-kB or NFkB) regulatory element. The presence of nuclear NF-kB DNA binding activity (as detected by electrophoretic mobility shift assay [EMSA]) is consistent with luciferase reporter activity; these reporter mice identify NF-kB transcriptional activity in any tissue. These transgenic mice may be useful in studies of immunology, cellular signaling, signal transduction, apoptosis, and transcription factor function.
002938	B6.129-Kdr^tm1Jrt/J	Repository-Cryopreserved
	Mice homozygous for the Kdr^tm1Jrt targeted mutation (formerly called Flk1) die at ~E8.5-E9.5 due to defects in hematopoietic and endothelial development. Embryos lack blood islands at E7.5 and fail to form organized blood vessels. There is severe reduction in hematopoietic progenitor cells.
006497	B6.129-Skil^tm2Spw/J	Repository-Cryopreserved
	Mice homozygous for this targeted mutation (called "Sno^ex1" in the primary reference) are viable and fertile with no reported gross morphological defects. Although the deletion of exon 1 leads to complete absence of the mature full-length protein in immunoblots of brain and embryonic tissues, a truncated 3'-end RNA species is derived from downstream coding sequence. Homozygotes exhibit T cell proliferation/activation defects, which can be rescued by treatment with anti-TGF-beta antibodies or exogenous interleukin-2. Homozygous deletion also results in increased sensitivity to TGF-beta and altered growth properties of cultured mouse embryo fibroblasts (MEFs). These mutant mice may be useful in studies of T cell activation, T cell receptor stimulation and TGF-beta signaling.
002619	B6.129-Tgfb3^tm1Doe/J	Repository-Cryopreserved
	Mice homozygous for the Tgfb3^tm1Doe mutation are not viable. Mice exhibit cleft palate and possibly developmental defects in the lung.
002816	B6.129P2-Il2rb^tm1Mak/J	Repository-Cryopreserved
	Mice homozygous for the Il2rb^tm1Mak targeted mutation have dysfunctional T and B cell compartments. Effects of the mutation include myeloproliferative disorder, splenomegaly and lymphoadenopathy by 3 weeks of age. Mice have high serum immunoglobulins G1 and E and autoantibodies leading to hemolytic anemia. Lifespan is approximately 12 weeks.
002405	B6.129P2-Ncam1^tm1Cgn/J	Repository-Cryopreserved
	Mice homozygous for the Ncam1^tm1Cgn targeted mutation show a 10% reduction in overall brain weight and 36% reduction in olfactory bulb size. Motor end plates were 14% smaller in NCAM-deficient mice compared to controls, and the formation of junctional folds was delayed. They also show deficits in spatial learning and in the amount of protein-bound alpha-(2,8)-linked polysialic acid. Both homozygous and heterozygous mutant mice are reportedly more aggressive than wildtype controls.
002219	B6.129P2-Tgfa^tm1Ard/J	Repository-Cryopreserved
	Mice homozygous for the Tgfa^tm1Ard mutation develop normally, are of normal size, weight, and health, and are fertile. They display a pronounced waviness in the coat and whiskers, and dramatic derangement of the hair follicles. Older homozygous mice occasionally show some corneal inflammation that may be the result of a defect in wound healing.
005963	B6.129S1-Csf2rb2^tm1Cgb Csf2rb^tm1Clsc/J	Repository-Cryopreserved
	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.
002984	B6.129S1-Il12rb1^tm1Jm/J	Repository-Cryopreserved
	Mice homozygous for the Il12rb^tm1Jm targeted mutation are viable and fertile. Con A-activated splenocytes from homozygous mutant mice express only low affinity IL12-binding sites and fail to proliferate or produce interferon gamma in response to IL12. In addition, NK lytic activity in response to IL12 is defective. In vivo immune responses to endotoxin are also impaired.
007016	B6.129S1-Irak3^tm1Flv/J	Repository-Cryopreserved
	Homozygotes are viable and fertile. Mice exhibit increased cytokine production upon TLR/IL1 stimulation and bacterial challenge, and show increased inflammatory responses to bacterial infection. Endotoxin tolerance is significantly reduced. Absence of gene expression was confirmed by Western blot using an antibody directed against the C terminus of the gene.
007017	B6.129S1-Ripk2^tm1Flv/J	Repository-Cryopreserved
	Homozygotes are viable and fertile and do not display any gross physical or behavioral abnormalities. Cytokine production in macrophages is reduced upon stimulation with lipopolysaccharide, peptidoglycan and double-stranded RNA, but not with bacterial DNA. Deficient cells are also hyporesponsive to signalling through IL1 and IL18 interleukin receptors, and deficient for signalling through NOD (nucleotide-binding oligomerization domain) proteins. T cells show severely reduced NFKB (nuclear factor of kappa light chain gene enhancer in B-cells) activation, IL2 production and proliferation on T cell receptor (TCR) engagement, and impaired differentiation to T-helper subtype 1 (T_H1)cells. Western blot analysis of thymocytes demonstrates the absence of protein in homozygous mutant mice.
007020	B6.129S1-Tlr1^tm1Flv/J	Repository-Cryopreserved
	Homozygotes are viable and fertile. IL6 production is significantly impaired in homozygous macrophages treated with Borrelia burgdorferi's OspA (outer-surface lipoprotein). No expression products from the gene are found in either lipopolysacharide (LPS)-treated or untreated bone marrow-derived macrophages, as assayed by RT-PCR. This strain may be useful in vaccine development.
002612	B6.129S2-Bmp4^tm1Blh/J	Repository-Cryopreserved
	Mice homozygous for the Bmp4^tm1Blh targeted mutation mutation die early in embryogenesis. Fifteen to twenty percent of heterozygous mice show developmental defects including polydactyly, craniofacial defects, and cystic kidneys. Heterozygotes have also been reported to show eye abnormalities.
002248	B6.129S2-Gzmb^tm1Ley/J	Repository-Cryopreserved
	Mice homozygous for the Gzmb^tm1Ley mutation are viable and fertile. Lymphopoiesis and peripheral lymphoid tissue development is normal. T cell responses to mitogenic (Con A and IL2) and allogeneic (mixed lymphocyte culture) stimulation are unaffected. There is a 10-fold reduction in condensation of chromatin resulting in nuclear crescents and pyknosis when Gzmb^tm1Ley CTL are used as effectors. Thus, activated CTL from homozygous mice are deficient in the early induction of DNA fragmentation and apoptosis in allogeneic target cells. Formerly called Ctla1.
002220	B6.129S2-Tgfb1^tm1Doe/J	Repository-Cryopreserved
	It has been reported that mice homozygous for Tgfb1^tm1Doe mutation develop normally but die approximately two to three weeks after birth. It was also reported that this strain shows a lower than expected number of homozygous births (~14% from heterozygous matings on a mixed genetic background) suggesting that in utero death may occur (See Husbandry). Homozygous mice usually die within a few days of the onset of a wasting syndrome. Death is due to a massive inflammatory cell response and tissue necrosis. A multifocal mixed inflammatory cell infiltration occurs into numerous organs, particularly the heart and stomach. Heterozygous mice do not differ from normal wildtype littermates. This strain may provide a model for human immune and inflammatory diseases such as autoimmune disease, transplant rejection and graft versus host reactions.
002275	B6.129S4-Ntf3^tm1Jae/J	Repository-Cryopreserved
	Mice homozygous for the Ntf3^tm1Jae targeted mutation are smaller than their normal littermates and most die shortly after birth. Survivors die prior to weaning. They display limb ataxia, an inability to position the limbs properly when attempting to move, and there is a tendency for all four limbs to intermittently stiffen in an extensor posture. Autopsy showed all peripheral ganglia markedly smaller in the mutant. Spinal proprioceptive afferents and their peripheral sense organs are completely absent. Heterozygous mice appear normal; however, the number of muscle spindles in heterozygotes is half that of normal wildtype siblings. There is approximately a 50% reduction in the sympathetic superior cervical ganglion (SCG) neurons caused by excessive apoptosis of sympathetic neuroblasts during neurogenesis.
003541	B6.129S4-Ntf3^tm2Jae/J	Repository-Cryopreserved
	This strain has loxP sites located on either side of the Ntf3 exon 2. Mice homozygous for this allele are viable, fertile and without behavioral abnormalities. If this strain is crossed with a transgenic strain bearing Cre recombinase, expression of the Ntf3 gene in offspring can be blocked in a tissue-specific manner depending on the promoter controlling the recombinase. Strains under the control of the rat nestin promoter block expression in the central nervous system; see strains 002275 and 002276.
004197	B6.129S6-Rac2^tm1Mddw/J	Repository-Cryopreserved
	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 descriiption on the strain data sheet
003246	B6.129S7-Tnfrsf1b^tm1Imx/J	Repository-Cryopreserved
	Mice homozygous for a Tnfrsf1b^tm1Imx targeted mutation (formerly Tnfr2^tm1Imx, p75 deficient) are viable and fertile. T cells from homozygous mutant mice display defects in activation induced cell death in vitro and dramatically elevated levels of circulating Tnf following systemic challenge with LPS. Pulmonary neutrophil influx is exacerbated in p75 deficient mice in a model of hypersensitivity pneumonitis.
008577	B6.129X1-Gpr65^tm1Witt/J	Repository-Cryopreserved
	Homozygous targeted mutant mice have thymocytes and splenocytes that, studied in vitro, are insensitive to pH-dependent cAMP production. Despite significant in vitro defects in the acidic pH-induced cAMP production, a preliminary examination of homozygous animals has not revealed any major abnormalities in the development of the immune system or in its major functions. A green fluorescent protein (GFP) insertion acts as a marker for cells that normally express the gene. This strain may be helpful in elucidating the role of this and other G protein-coupled receptors in the regulation of immune cell responses in acidic microenvironments.
005912	B6.Cg-Il10^tm1Cgn (D3Mit49-D3Mit348)/Lt	Repository-Cryopreserved
	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.
002993	B6.Cg-Kitl^Sl-18H/EiJ	Repository-Cryopreserved

000124	B6.Cg-Kitl^Sl Krt71^Ca/J	Repository-Cryopreserved
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. Kitl^Sl/Kitl^Sl-d are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with adva ..... For more information please see the full descriiption on the strain data sheet
002863	B6.Cg-Tgfa^wa1/J	Repository-Cryopreserved
	Mice homozygous for the Tgfa^wa1 spontaneous mutation are recognizable at 2 or 3 days of age by their curly whiskers. The first coat is strongly waved and straight in later coats. Most of the whiskers also become straight, but the guard hairs are curved and shorter than normal. Some homozygotes have eyelids open at birth. Ventricular enlargement and striatal reduction is observed in adult homozygous wa1 mice. The phenotype is more severe in males. In addition, adult males exhibit reduced hippocampal volume and impaired auditory and contextural fear learning. Both sexes demonstrate an abnormal fear response. Peripubertal mice do not exhibit behavioral deficits despite slight forebrain structural abnormalities. (Koshibu K, et al., 2005)
004753	B6.Cg-Tg(Il1rn)1Dih/J	Repository-Cryopreserved
	These transgenic mice overexpress the secreted mouse Il1rn under the control of endogenous regulatory elements. The transgene contains the sequence encoding the secreted protein with a point mutation (G to A) in exon 3. These mice have an estimated 8 copies of the transgene in tandem array. Northern blot analysis of liver tissue following lipopolysaccharide (LPS) endotoxin challenge detects overexpression. RT-PCR analysis of corneal tissue detects higher levels of gene product (mRNA) than wildtype controls. The Donating Investigator reports that hemizygous mice are viable and fertile, whereas homozygous mice are sickly and die prematurely. Transgenic mice are less susceptible to LPS challenge than wildtype controls, but are more susceptible to experimental Listeria monocytogenes infection. Following endotoxin (LPS) challenge serum IL-1 levels are higher. Mice hemizygous for the transgene exhibit an intermediate susceptibility. Severity of stromal keratitis caused by herpes simpl ..... For more information please see the full descriiption on the strain data sheet
006101	B6.Cg-Tg(TRE/Prl-luc)31FlvRinc/J	Repository-Cryopreserved
	Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Naïve (unstimulated) cells from transgenic mice show no luciferase activity. When activated via addition of phorbol myristate acetate (PMA) plus ionomycin, cell populations from hemizygous mice exhibit high luciferase transcriptional activity in CD4⁺ T cells. Identically treated single-positive CD8⁺ T cells have lower transcriptional activity, while no luciferase is observed in B cell populations. Interleukin-2 transcriptional activators (anti-CD3 and ConA) also promote similar cell-specific patterns of reporter transcription. Luciferase expression is cyclosporine sensitive. Nuclear proteins isolated from hemizygous splenocytes show AP-1 specific binding to the transgenic TRE domain. This reporter transgene faithfully identifies AP-1 transcriptional activity both in vivo and in vitro. These mice may be useful in studies of immu ..... For more information please see the full descriiption on the strain data sheet
006086	B6.SJL-Tg(HBB-GH1)420King/J	Repository-Cryopreserved
	Mice hemizygous for this transgene are viable. While males are fertile, transgenic females are unreliable breeders and mothers. Homozygotes are sterile. In both fetal and adult tissues, erythroid-specific expression of the transgene is observed. Transgenic mice have 120-150% greater mature body mass and increased bone mass. The donating investigator also reports transgenic mice have increased dermatological stiffness and toughness. Transgenic mice have a characteristic coat with few guard hairs compared to wildtype littermates. These mice may be useful in studies of bone formation and development, dermatology, and acromegaly.
006011	B6;129-Ly9^tm1Mckn/J	Repository-Cryopreserved
	Mice homozygous for the targeted mutation are viable, fertile, and do not display any gross anatomical or behavioral abnormalities. FACS analysis of splenocytes confirms homozygous mice do not express the endogenous protein. When stimulated with anti -CD3, splenocytes cultured from homozygous mice show significant early T cell activation defects (proliferation and IL-2 production). When stimulated with anti-TCR and anti-CD28, CD4⁺ T splenocytes cultured from homozygous mice exhibit mild defects in Th2 cytokine production, but respond normally to cytokine stimulation. These mutant mice may be useful in studies of innate and adaptive immunity, lymphocyte signaling/costimulation, T cell activation, Th1/Th2 cytokine function, and CD2/SLAM family signal transduction.
004101	B6;129P-Ccr4^tm1Pwr/J	Repository-Cryopreserved
	Mice that are homozygous null for the Ccr4 gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Ccr4 gene product (mRNA or protein) is detected. Although some normal responses to bacterial lipopolysaccharide (LPS) administration are observed (shivering and lethargy), these mice are resistant to LPS-induced lethality. Significantly lower levels of serum tumor necrosis factor alpha and interleukin 1 beta are observed in response to LPS injection. Splenocytes and thymocytes show no chemotactic response to Ccr4 ligands and diminished macrophage levels are observed in thioglycollate-elicited peritoneal cells.
002398	B6;129P2-Csf3^tm1Ard/J	Repository-Cryopreserved
	Mice homozygous for the Csf3^tm1Ard targeted mutation are viable and fertile but are characterized by chronic neutropenia. Peripheral blood neutrophil levels of homozygotes are 20 to 30% of wildtype. There is a 50% reduction of granulocyte, macrophage and blast progenitor cells in marrow of homozygous mice and an impaired resistance to infection with Listeria monocytogenes.
003284	B6;129S1-Il1rap^tm1Roml/J	Repository-Cryopreserved
	Interleukin-1 receptor accessory protein (Il1rap)-null mice are viable and fertile. They exhibit loss of Il-1 receptor mediated signal transduction. Treatment of these mutant mice with IL-1 Alpha or IL-1 Beta results in no detectable increase in IL-6 levels in serum and fails to induce increased expression of E-selectin mRNA.
003666	B6;129S1-Map2k4^tm1Liz/J	Repository-Cryopreserved
	Mice that are homozygous null for the Map2k4(SEK1, JNKK, or MKK4) gene exhibit liver abnormalities and suffer lethality before embryonic day 14.5. Histological examination reveals a reduced number of hepatocytes and enlarged, hemorrhaging sinuses. The donating investigator speculates that embryo death results from anemia brought on by massive bleeding. SEK1 is an enzyme in the stress-activated MAP kinase pathway.
002247	B6;129S2-Gzmb^tm1Ley/J	Repository-Cryopreserved
	Mice homozygous for the Gzmb^tm1Ley mutation are viable and fertile. Lymphopoiesis and peripheral lymphoid tissue development is normal. T cell responses to mitogenic (Con A and IL2) and allogeneic (mixed lymphocyte culture) stimulation are unaffected. There is a 10-fold reduction in condensation of chromatin resulting in nuclear crescents and pyknosis when Gzmb^tm1Ley CTL are used as effectors. Thus, activated CTL from homozygous mice are deficient in the early induction of DNA fragmentation and apoptosis in allogeneic target cells. Formerly called Ctla1.
002257	B6;129S2-Lta^tm1Dch/J	Repository-Cryopreserved
	Mice homozygous Lta^tm1Dch targeted mutation are viable and fertile. Homozygous mutant mice show abnormal development of peripheral lymphoid organs with no detectable popliteal, inguinal, para-aortic, mesenteric, axillary, or cervical lymph nodes, and no detectable Peyer's patches. Morphological changes in the spleen white pulp were accompanied by alterations in T and B cell content. CD4⁺ and CD8⁺ T cells counts in peripheral blood are normal but there is a four-fold increase in B cells. Neutrophil, monocyte, and platelet counts are normal. The thymus contains normal numbers of CD4⁺CD8⁺, CD4⁺, CD8⁺, and CD4^-CD8^- T cells. Splenic T cells develop normal MHC class I and class II-restricted allocytotoxic responses. Also known as tumor necrosis factor beta, Tnfb.
002481	B6;129S2-Ntrk3^tm1Bbd/J	Repository-Cryopreserved
	Mice homozygous for this Ntrk3^tm1 targeted mutation (commonly referred to as trkC) die by 2-3 weeks of age. Homozygous mutant mice lack proprioceptive and cochlear neurons and have a reduction in vestibular neurons.
002462	B6;129S4-Il2ra^tm1Dw/J	Repository-Cryopreserved
	Mice homozygous for the Il2ra^tm1Dw targeted mutation are are characterized by a lymphoproliferative disorder, hemolytic anemia, and an inflammatory bowel disease beginning at approximately 9 weeks of age; also known as p55 gene chain, Ly43, CD25.
002296	B6;129S7-Il7r^tm1Imx/J	Repository-Cryopreserved
	Mice homozygous for the Il7r^tm1Imx targeted mutation are viable and fertile. Newborn and young adult homozygous mutant mice have dramatically reduced thymic and splenic lymphoid cellularity in both B and T cell compartments. T cell development is affected prior to surface expression of CD4 and CD8 and prior to the initiation of T cell receptor beta chain rearrangement. B cell development is through pre-pro-B cells (Cd43⁺ HSA^dull). The phenotype in the mouse resembles human interleukin-2 receptor gamma deficiency (XSCID). IL2Rgamma has been shown to be a necessary component of the IL7R providing the biochemical basis for this condition.
002402	B6;129S7-Lifr^tm1Imx/J	Repository-Cryopreserved

000553	B6EiC3Sn a/A-Egfr^wa2 Wnt3a^vt/J	Repository-Cryopreserved
	Mice homozygous for the spontaneous waved 2 mutation (Egfr^wa2) are recognizable at 2 to 3 days by curly whiskers. The first coat is waved but later coats are not; vibrissae usually remain curled and the guard hairs curved. Some homozygotes have eyelids open at birth. Fertile mutant females have impaired lactation. Mice homozygous for the vestigial tail spontaneous mutation (Wnt3a^vt) have very short tails, few presacral vertebrae, and abnormal formation of the lumbar vertebrae.
002229	C.129P2(B6)-Il2^tm1Hor/J	Repository-Cryopreserved
	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 descriiption on the strain data sheet
003017	C.129S1-Il12rb1^tm1Jm/J	Repository-Cryopreserved
	Mice homozygous for the Il12rb^tm1Jm targeted mutation are viable and fertile. Con A-activated splenocytes from homozygous mutant mice express only low affinity IL12-binding sites and fail to proliferate or produce interferon gamma in response to IL12. In addition, NK lytic activity in response to IL12 is defective. In vivo immune responses to endotoxin are also impaired.
003480	C.129S2(B6)-Il4^tm1Gru/J	Repository-Cryopreserved
	This strain was made using gene targeting in embryonic stem cells to modify the Il4 locus by knocking-in a transmembrane domain. Expression of Il4 in a membrane-bound form provides a novel method for the identification and characterization of Il4-producing cells.
006134	C.129S4(B6)-Cxcl10^tm1Adl/J	Repository-Cryopreserved
	Homozygous mice are viable, fertile, and have no overt morphological or developmental abnormalities. No endogenous gene expression is observed in bone marrow-derived macrophages before or after IFN-gamma stimulation. Homozygous mice have defective T cell responses, including impaired proliferation and IFN-gamma secretion following antigenic challenge (129Sv background). In experimental models of T helper-1 (Th1)-mediated immune responses, homozygous-deletion leads to diminished immune function; contact hypersensitivity is reduced (129Sv background) and diminished threshold for disease expression in experimental autoimmune encephalomyelitis (EAE, human model of multiple sclerosis) (C57BL/6 background). After injection with a neurotropic coronavirus MHV, null mice (on a B6;129Sv background) exhibit impaired viral clearance, decreased CD4⁺/CD8⁺ infiltration into the brain, and are protected from viral-induced demyelination. Similarly, homozygous mice (on a C57BL/6 ba ..... For more information please see the full descriiption on the strain data sheet
003830	C.129S4(B6)-Mif^tm1Dvd/J	Repository-Cryopreserved
	Mice that are homozygous null for the Mif gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Mif gene product (mRNA or protein) is detected. While null mice exhibit signs of endotoxemia in response to intraperitoneally injected LPS (25 mg/kg), they are resistant to its lethal effects. Plasma levels of tumor necrosis factor alpha assayed after LPS administration is half that observed in wildtype mice.
003169	C.129S4-Il2rg^tm1Wjl/J	Repository-Cryopreserved
	Mice homozygous for the Il2rg^tm1Wjl targeted mutation are viable and fertile. Mutant mice have hypoplastic thymuses with a 10-fold reduction in the absolute number of lymphocytes. They have a limited number of mature splenic B and T cells, lack NK cells and Peyer's patches, and development of gut-associated intraepithelial lymphocytes is diminished. In vitro studies show defects in NK activity, IL4-directed Ig class switching of thymocytes, and thymocyte mitogenic responses.
002228	C3.129P2(B6)-Il2^tm1Hor/J	Repository-Cryopreserved
	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 descriiption on the strain data sheet
003968	C3Bir.129P2(B6)-Il10^tm1Cgn/LtJ	Repository-Cryopreserved
	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 descriiption on the strain data sheet
000291	C3FeLe.Cg-a/a Hm Kitl^Sl Krt71^Ca-J/J	Repository-Cryopreserved
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by

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