JAX Mice Database - CD Antigens, Antigen Receptors, and Histocompatibility Markers

Search Criteria: Research Area is "Immunology and Inflammation Research: CD Antigens, Antigen Receptors, and Histocompatibility Markers"

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

JAX^® Mice Strains

Stock Number	Strain Name Strain Description	Standard Supply
000659	C3H/HeJ	Level 1
	C3H/HeJ mice are used as a general purpose strain in a wide variety of research areas including cancer, immunology and inflammation, sensorineural, and cardiovascular biology. C3H/HeJ mice and all other Jackson substrains are homozygous for the retinal degeneration 1 mutation (Pde6b^rd1), which causes blindness by weaning age. There is also a high incidence of hepatomas in C3H mice (reportedly 72-91% in males at 14 months, 59% in virgin females, 30-38% in breeding females). Despite the lack of exogenous mouse mammary tumor virus (MMTV), virgin and breeding females may still develop some mammary tumors later in life. C3H/HeJ mice, fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat), fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 00066 ..... For more information please see the full descriiption on the strain data sheet
000465	B10.BR-H2^k H2-T18^a/SgSnJ	Level 2
	Some phenotypic parameters of the B10.BR-H2^k H2-T18^a/SgSnJ mice may have changed recently relative to the strain's previous performance. In order to confirm that a change had occurred and in order to better characterize any differences that may have arisen, animals were recovered from cryo-preserved embryos of the strain (Stock No. 004804) that had been frozen in 1991, and the two lines of B10.BR-H2^k H2-T18^a/SgSnJ were compared. Differences between the two strains have been identified in the CD4/CD8 ratios among several cell populations, and in some dendritic cell populations. As more information is gathered, this website will be updated. Both colonies of B10.BR-H2^k H2-T18^a/SgSnJ (Stock No's. 000465 and 004804) may exhibit white belly ..... For more information please see the full descriiption on the strain data sheet
000457	B10.RIII-H2^r H2-T18^b/(71NS)SnJ	Level 2
	This congenic strain develops chronic and relapsing experimental autoimmune encephalomyelitis (EAE) after immunization with myelin basic protein (MBP). Susceptibility is associated with the major histocompatibility complex (MHC) allele, H2^r, the T cell receptor V β8 chain, and other non MHC loci. This strain also is susceptible to induction of collagen-induced arthritis.
001162	B6(C)-H2-Ab1^bm12/KhEgJ	Level 2

000406	B6.PL-Thy1^a/CyJ	Level 2
	This C57BL/6J congenic strain is useful because it carries the T lymphocyte specific Thy1^a (Thy1.1) allele. Donor T cells can be easily distinguished from recipient T cells by both flow cytometric and histological analysis using appropriate antibodies.
002014	B6.SJL-Ptprc^a Pepc^b/BoyJ	Level 2
	This is a congenic strain used in transplant studies because it carries the differential B cell antigen originally designated Ly5.1 and CD45.1 The current use of the Ptprc designation for Cd45 and Ly5 was based on work in humans following the report of Charbonneau and colleagues who first showed that a protein-tyrosine phosphatase (human placental protein-tyrosine phosphatase 1B) was homologous to the CD45 protein. Ptprc is one of a family of protein-tyrosine phosphatase genes involved in the regulation of cell growth. The b allele is normally present in the BALB and C57BL inbred strains.
000469	B10.A-H2^a H2-T18^a/SgSnJ	Level 3

004804	B10.BR-H2^k H2-T18^a/SgSnJJrep	Level 3
	Some phenotypic parameters of the B10.BR-H2^k H2-T18^a/SgSnJ (Stock No. 000465) mice may have changed recently relative to the strain's previous performance. In order to confirm that a change has occurred and in order to better characterize any differences that may have arisen, animals were recovered from cryopreserved embryos of the strain (B10.BR-H2^k H2-T18^a/SgSnJJrep Stock No. 004804) that had been frozen in 1991, and the two lines of B10.BR-H2^k H2-T18^a/SgSnJ were compared. Differences between the two strains have been identified in the CD4/CD8 ratios among several cell populations, and in some dendritic cell populations. As more information is gathered, this website will be updated. Both colonies of B10.BR-H2^k H2-T18^a/SgSnJ (000465 and 004804) may exhibit whit ..... For more information please see the full descriiption on the strain data sheet
002024	B10.D1-H2^q/SgJ	Level 3

000461	B10.D2-Hc⁰ H2^d H2-T18^c/oSnJ	Level 3
	This congenic strain carries the H2^d haplotype from DBA/2J following six generations of backcrossing to C57BL/10Sn. This strain still carries the Hc⁰ allele from DBA/2J, making them serum C5 deficient. Mice have increased susceptibility to certain pathogens and impaired chemotactic responses of neutrophils. Allograft rejection is prolonged. The following inbred strains are also homozygous for the Hc⁰ allele: A/HeJ (Stock No. 000645), AKR/J (Stock No. 000648), DBA/2J (Stock No. 000671), NOD/LtJ (Stock No. 001976), NZB/BlNJ (Stock No. 000684), and SWR/J (Stock No. 000689).
000463	B10.D2-Hc¹ H2^d H2-T18^c/nSnJ	Level 3

000458	B10.PL-H2^u H2-T18^a/(73NS)SnJ	Level 3

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.
003303	C.Cg-Tg(DO11.10)10Dlo/J	Level 3
	Mice carrying the MHC class II restricted rearranged T cell receptor transgene, Tg(DO11.10)10Dlo, react to ovalbumin (OVA) peptide antigen. Intraperitoneal administration of OVA to transgenic mice results in a rapid deletion of the immature CD4⁺ CD8⁺ TCR^lo thymocytes with progression to mature thymocytes. Apoptosis of cortical thymocytes within 20 hours of treatment indicates that apoptosis in important in the development of antigen-induced tolerance. Use of this rearranged T cell receptor transgene requires H2^d background.
000438	C3.SW-H2^b/SnJ	Level 3
	Male mice from the C3.SW-H2^b/SnJ congenic strain are predisposed to maturity-onset impairment of glucose tolerance and hyperinsulinemia with some mice exhibiting hyperglycemia. Symptoms occur much later, between 5 and 8 months of age, than most of the single gene obese and diabetic strains. In addition, male mice are susceptible to the diabetogenic effects of multiple low doses of streptozotocin (40 mg/kg BW.day X 5).
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
004194	C57BL/6-Tg(TcraTcrb)425Cbn/J	Level 3
	These transgenic mice express the mouse alpha-chain and beta-chain T-cell receptor that pairs with the CD4 coreceptor and is specific for chicken ovalbumin 323-339 in the context of I-A b. Homozygous mice are viable and fertile. In these mice there is a four-fold increase in the CD4 to CD8 peripheral T-cell ratio, and lymph node T-cells demonstrate a dose-dependent proliferative response to the specific ovalbumin ligand. These transgenic mice are useful for studying in vivo T-cell biology such as TCR-ligand interactions, T-cell activation, thymic selection, cross-presentation of antigens, process of thymic selection and central and peripheral T-cell tolerance and induction.
000471	A.SW-H2^s H2-T18^b/SnJ	Level 4

004650	B6.129-Tlr2^tm1Kir/J	Level 4
	Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by Western blot analysis of isolated peritoneal macrophages. Bone marrow derived macrophages do not respond to spirochete (Borrelia burgdorferi) lipoprotein challenge, although non-lipoprotein sonicate stimulates activation. Arthritis due to B. burgdorferi infection, as assessed by rear ankle swelling, is more severe in mutant mice. Tissues of infected mutants can contain up to 100 times higher bacteria levels than those found in wildtype littermates. Elevated spirochete numbers persist 8 weeks post-infection. Homozygotes do not produce TNF-alpha or IL-6, and do not develop symptoms of illness when treated with leptospiral (Leptospira interrogans) lippolysaccharide (LPS). This mutant mouse strain may be useful in studies of host response to bacterial endotoxins such as septic shock.
002118	B6.129P2-Tcrb^tm1Mom/J	Level 4
	Mice homozygous for the Tcrb^tm1Mom targeted mutation are viable and fertile. Mice are deficient in alpha beta T-cell receptor. The total number of cells in the thymus is ~8% that of wildtype; CD4⁺CD8⁺ cells ~6% of wildtype. The proportion of CD4^-CD8^- (IL2 receptor positive) cells increases to about 50% of the total cell number. Alpha beta thymocyte differentiation is blocked at an earlier stage than the Tcra^tm1Mom strain. There is normal differentiation of gamma delta thymocytes. Mice may develop inflammatory bowel disease beginning at ~4-6 months of age.
002120	B6.129P2-Tcrd^tm1Mom/J	Level 4
	Mice homozygous for the Tcrd^tm1Mom targeted mutation are viable and fertile. Gamma delta T-cell receptor expression is deficient in all adult lymphoid and epithelial organs. There is normal development of the alpha beta T-cell lineage. Patterns of CD4⁺CD8^- and CD4^-CD8⁺ alpha beta T-cells are apparently normal. Mice do not develop inflammatory bowel disease.
002663	B6.129S2-Cd4^tm1Mak/J	Level 4
	Mice homozygous for the Cd4^tm1Mak targeted mutation have a significant block in CD4⁺ T-cell development; 90% of their circulating T-cells are CD8⁺. Cell surface expression of CD4 protein is not detected on thymocytes and lymph node cells from homozygous mice. Homozygous mutant mice also show a Class II restricted deficit in helper T-cell activity and other T-cell responses. This mutant mouse strain may be useful in studies of T cell development, susceptibility to viral infection and inflammation.
002665	B6.129S2-Cd8a^tm1Mak/J	Level 4
	Mice homozygous for the Cd8a^tm1Mak targeted mutation are deficient in functional cytotoxic T-cells; however, helper T-cell development and function is comparable to normal.
002116	B6.129S2-Tcra^tm1Mom/J	Level 4
	Mice homozygous mice for the Tcra^tm1Mom targeted mutation are viable and fertile. They are deficient in the alpha beta T-cell receptor. The thymus is devoid of CD4⁺CD8^- and CD4^-CD8⁺ cells. Normal numbers of CD4⁺CD8⁺ cells are retained without the IL2 receptor. There are normal numbers of CD4^-CD8^- cells. ~1% of the thymocytes express the gamma delta TCR. Mice may develop inflammatory bowel disease beginning at ~4-6 months of age.
001060	B6.C-H2^bm1/ByJ	Level 4

002930	C.C3-Tlr4^Lps-d/J	Level 4
	In addition to the Tlr4^Lps-d congenic interval from C3H/HeJ, this strain is also congenic for the wild type tyrosinase allele from C3H/HeJ on chromosome 7. This strain provides a tool for analysis of markers in the region and for examining functional effects of Lps^d on BALB/c, a strain susceptible to infection, neoplastic disease including the induction of plasmacytomas and other tumors.
003475	C57BL/6-Tg(HLA-A2.1)1Enge/J	Level 4
	Homozygous mice carrying the Tg(HLA-A2.1)1Enge transgene express significant quantities of the human class I MHC Ag HLA-A2.1 on cells from the spleen, bone marrow and thymus. Expression of this human class I molecule did not result in expansion of the number of cytotoxic T lymphocyte (CTL) precursors specific for other human class I Ag, HLA-B27 or HLA-A2.2. These transgenic mice have been used to identify hepatitic C virus (HCV) peptides expressing a sequence for HLA-A2.1 binding that are actually recognized by human A2.1-restricted CTLs. Thus, this transgenic model is important for the study of HLA-restricted CTL determinants and in potential development of a vaccine against HCV. *Note: copy number may be variable. Hemizygotes are tested for expression prior to distribution.
003831	C57BL/6-Tg(TcraTcrb)1100Mjb/J	Level 4
	These mice contain transgenic inserts for mouse Tcra-V2 and Tcrb-V5 genes. The transgenic T cell receptor was designed to recognize ovalbumin residues 257-264 in the context of H2K^b and used to study the role of peptides in positive selection and the response of CD8⁺ T cells to antigen. Like most TCR transgenics, these mice are somewhat immunodeficient.
000629	C57BL/6J-Lyst^bg-J/J	Level 4
	Mice homozygous for the beige-J spontaneous mutation (Lyst^bg-J) are identical to the original beige mutation (Lyst^bg). The phenotype closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syn ..... For more information please see the full descriiption on the strain data sheet
006500	129.NOD-(D17Mit175-H2)/J	Repository- Live
	129S1.NOD-H2^g7 congenic mice are viable, fertile, normal in size, do not display any gross physical or behavioral abnormalities and are diabetes free. Because targeted mutations frequently are made using 129 ES cells, this strain may be useful for identifying Idds in 129 strains.
000140	A.BY-H2^bc H2-T18^f/SnJ	Repository- Live
	Dr. George Snell, of The Jackson Laboratory, created this H2-congenic strain by crossing of mice of a non-inbred stock carrying the brachyury mutation (and therefore called BY) to mice of the A/Lilly inbred strain, then repeatedly backcrossing to the latter strain mice that proved resistant to A-derived tumors. A/Lilly was a subline of strain A that Snell obtained from the Lilly Company after the 1947 fire at The Jackson Laboratory; when it was learned that this strain was contaminated, Snell performed a single additional backcross to the A/WySn subline, taking it to generation N11 (Rodgers 2004; Klein 1989). The BY stock apparently was obtained from Dr. Dobrovolskaia-Zavadskaia, who described a short-tailed mouse sired by a gonadally-irradiated male; she believed the brachyury mutation not to have been caused by the radiation, but to have been a pre-existing spontaneous mutation (Dobrovoskaya-Zajadkaya 1927; Rodgers 2004). In a subsequent article, she described short tailed (b ..... For more information please see the full descriiption on the strain data sheet
000468	B10.A-H2^h2/(2R)SgSnJ	Repository- Live

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.
002761	B10.Cg-Tg(TcrAND)53Hed/J	Repository- Live
	Mice carrying the (TcrAND)53Hed transgene express a rearranged T-cell receptor (V alpha 11.1 / V beta 3) specific for the carboxy-terminal fragment of pigeon cytochrome c and the E^k molecule, resulting in a major subpopulation of T cells restricted to class II MHC proteins. There are an abnormally high percentage of mature CD4⁺CD8^- cells. The peripheral T-cell population is almost exclusively CD4⁺. The original C57BL/6 and SJL mixed background strain (Stock number 002408) was backcrossed to C57BL/10 to create this strain. Both strains are fixed for H2^b. Because C57BL/10 mice do not express I-E, this mouse must be crossed to a strain that expresses I-E^k to study the interaction of the transgenic T-cell receptor with the pigeon cytochrome c antigen. The lack of I-E^k expression in the transgenic line allows it to serve as a universal donor for crossing the transgene onto other strains expressing I-E^k< > ..... For more information please see the full descriiption on the strain data sheet
001953	B10.S-H2^s/SgMcdJ	Repository- Live

005717	B6(NOD) H2^g7-Sostdc1^shk/J	Repository- Live

003173	B6.129-Cd47^tm1Fpl/J	Repository- Live
	Mice homozygous for the targeted mutation are viable, fertile, and display no obvious phenotypic abnormalities. Homozygous mutant mice display normal blood counts except for a reduction in the CD3⁺ fraction of peripheral lymphocytes. Integrin-associated protein (IAP; CD47) expression in heterozygous mice was approximately 40% of wildtype. Intraperitoneal injection of virulent Escherichia coli kills IAP-deficient mice, indicating a defect in the host defense pathway. This response appears to be secondary to both delayed polymorphonuclear leukocyte (PMN) migration to the site of infection and to defective activation at the site.
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
006785	B6.129P2(C)-Cd19^tm1(cre)Cgn/J	Repository- Live
	Homozygous mutant mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Homozygotes have a deficiency in the B-1 subset of B-lymphocytes along with a concomitant reduction in serum IgM. Their ability to respond to T-cell-dependent antigens is severely impaired, and they fail to form splenic germinal centers. In addition to disrupting the targeted gene, the targeting construct also introduced a cre cassette into exon 2 of the targeted gene, effectively placing cre expression under the control of the endogenous promoter. The Cd19 promoter specifically directs cre expression at the earliest stages and throughout B-lymphocyte development and differentiation. Although homozygous mutant mice are Cd19-deficient, heterozygous mice are phenotypically normal, and can be used for specific deletion of loxP-flanked (floxed) targets in B-lymphocytes. In an attempt to offer alleles on well-characte ..... For more information please see the full descriiption on the strain data sheet
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.
003171	B6.129P2-Fcgr3^tm1Sjv/J	Repository- Live
	Mice homozygous for the Fcgr3^tm1Sjv targeted mutation, which eliminates the ligand-binding alpha chain of FcgammaRIII, are viable and fertile. Homozygous mutant mice lack NK cell-mediated antibody-dependent cytotoxicity, phagocytosis of IgG1-coated particles by macrophages, and IgG-mediated mast cell degranulation. They are resistant to IgG-dependent passive cutaneous anaphylaxis, and exhibit an impaired Arthus reaction.
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.
002122	B6.129P2-Tcrb^tm1Mom Tcrd^tm1Mom/J	Repository- Live
	Mice homozygous for both the Tcrb^tm1Mom and the Tcrd^tm1Mom targeted mutations express no alpha beta T-cell receptor nor any gamma delta T-cell receptor. Under certain housing conditions homozygous mutant mice develop mild inflammatory bowel disease.
003726	B6.129S-Cd14^tm1Frm/J	Repository- Live
	Mice that are homozygous null for Cd14 are viable and fertile. No Cd14 protein product is detected in thioglycollate elicited peritoneal (T-EP) macrophages by Western blot analysis. Unlike wildtype T-EP macrophages, T-EP macrophages derived from these animals fail to secrete TNF-alpha and IL-6 in response to lipopolysaccharide (LPS). Such a response is observed when Cd14 -null T-EP macrophages are exposed to whole bacteria (in the form of E. coli bioparticles), apparently by a Cd14-independent mechanism.
005763	B6.129S1-Nod2^tm1Flv/J	Repository- Live
	Homozygous mice are viable and fertile with normal lymphoid and myeloid cellularity and no intestinal inflammation up to 6 months of age. Homozygotes do not express the targeted gene in spleen or intestinal crypts. Null mice, as well as antigen presenting cells derived from them, lack the protective immunity (IgG1, interleukin-6, and NF-kappaB-related responses) normally afforded by endogenous protein recognition of its ligand, bacterial muramyl dipeptide (MDP). Mice homozygous for the mutation have increased susceptibility to oral (intragastric) bacterial challenge and diminished cryptdins. This mouse may be useful in studies of Crohn's disease and other inflammatory bowel diseases, innate immunity, signal transduction, and bacterial susceptibility.
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
006144	B6.129S2(C)-Itgae^tm1Cmp/J	Repository- Live
	Mice that are homozygous for this targeted mutation are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. No endogenous gene expression is detected in intraepithelial lymphocytes by FACS analysis or on TGF-beta1-treated splenocytes by immunoprecipitation. Homozygous null mice exhibit reduced numbers of intestinal intraepithelial lymphocytes and lamina propria lymphocytes. These mice may be useful in studies of the immune system, including T cell function. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
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
002666	B6.129S2-Cd28^tm1Mak/J	Repository- Live
	Mice homozygous for the Cd28^tm1Mak targeted mutation exhibit normal development of T and B cells, but have an impaired response to lectins. Other characteristics of homozygous mutant mice include decreased IL2 receptor expression, reduced basal Ig levels, low titers of IgG1 and IgG2b but increased IgG2a, reduced activity of T helper cells and diminished Ig class switching after infection with vesicular stomatitis virus. Infection of mice with lymphocytic choriomeningities virus creates induced and delayed-type hypersensitivity response in cytotoxic T cells.
002770	B6.129S2-Cd40lg^tm1Imx/J	Repository- Live
	Mice homozygous for the targeted mutation are viable and fertile. Homozygous mutant mice show no overt phenotypic abnormalities. Percentages of B and T cell subpopulations is normal. Homozygotes do show selective deficiencies in humoral immunity (low basal serum isotype levels and undetectable IgE) as well as abnormal secondary antigen-specific responses to immunization with a thymus-dependent antigen. The phenotype of the mice resembles human X-linked hyper IgM syndrome.
003584	B6.129S2-H2^dlAb1-Ea/J	Repository- Live
	Mice that are homozygous null for MHC class II genes H2-Ab1, H2-Aa, H2-Eb1, H2-Eb2, H2-Ea are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. MHC class II gene products (mRNA or protein) are not detected. A dramatic decrease is observed in the number of CD4 positive T cells in thymus, spleen and lymph nodes. This strain should serve as a suitable recipient of xenogenic Class II MHC transgenes allowing the engineering of mouse models of human MHC Class II-associated diseases. 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.
002704	B6.129S4-Cd247^tm1Lov/J	Repository- Live
	Mice homozygous for the Cd3z^tm1Lov targeted mutation are viable and fertile. Homozygous mutant mice exhibit impaired T-cell development and function.
003610	B6.129S4-Cd80^tm1Shr Cd86^tm2Shr/J	Repository- Live
	Cd80/Cd86-mediated signaling is critical to germinal center formation and Ig class switching in vivo. Mice homozygous for both the Cd80 (B7-1) and Cd86 (B7-2) targeted mutations are viable, fertile and have a normal life span. Homozygous null Cd80/Cd86 mice fail to generate antigen specific IgG1 and IgG2a responses. During the postimmunization period (seven-10 days) they have smaller spleens devoid of germinal centers. Unimmunized null mice exhibit a three to five fold reduction in total serum immunoglobulin and IgG2a. Levels of IgG1 are also reduced five to 10 fold. Levels of IgM and IgG3 are elevated three to five fold. When immunized, antigen specific IgG1 and IgG2a isotype levels are 0.1% that of wild-type levels. Levels remain low even when immunization is performed with adjuvent. This strain is also resistant to myelin oligodendrocyte glycoprotein (MOG) 35-55 peptide-induced experimental autoimmune encephalomyelitis (EAE), a T cell-mediat ..... For more information please see the full descriiption on the strain data sheet
003611	B6.129S4-Cd80^tm1Shr/J	Repository- Live
	Cd80 (B7-1) null mice are viable and fertile. They possess normal numbers of B and T lymphocytes but exhibit a diminished mixed lymphocyte response. Following immunization, antigen specific IgG1, IgG2a and IgM isotypes are 25%-50% that of wild type levels. Survival of certain tissue allografts are slightly prolonged in Cd80 null mice.
003609	B6.129S4-Cd86^tm1Shr/J	Repository- Live
	Cd86 (B7-2) null mice are viable and fertile. Unimmunized mice have normal levels of serum immunoglobulin and normal numbers of B and T lymphocytes. Upon intravenous immunization without adjuvant, they fail to form germinal centers or undergo isotype switching and antigen specific IgG1 and IgG2a isotypes are found to be 5% that of wild type levels. When the immunization route is subcutaneous, IgG1 and IgG2a levels are the same as in wild type mice.
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
002867	B6.129S4-Icam1^tm1Jcgr/J	Repository- Live
	Mice homozygous for the Icam1^tm1Jcgr targeted mutation are viable and fertile. The phenotype is similar to C57BL/6J-Icam1^tm1Bay (Stock No. 002127) but are reported to be less leaky. Characteristics include longer lifespan and nephritis with no apparent lung involvement.
006122	B6.129S4-Mbl1^tm1Kata Mbl2^tm1Kata/J	Repository- Live
	Mice homozygous for both mannose-binding lectin (MBL)-A and MBL-C targeted mutations (termed MBL-null) are viable, fertile, and normal in size with no obvious developmental defects. Histological examination of multiple organs from 6-10 week old mice shows no abnormalities. MBL-null mice have no endogenous gene expression in liver (the principal site of MBL synthesis) and no protein detectable in serum. While the classical complement pathway is unaffected in MBL-null mice, the lectin-dependent complement pathway is non-functional. MBL-null mice have increased mortality following intravenous injection of S. aureus associated with abnormal serum levels of TNFalpha and IL-6 (decreased at 2h, elevated at 24h post injection). Cyclophosphamide-induced febrile neutropenic MBL-null mice inoculated with S. aureus have greatly increased susceptibility to abscess formation in kidney, liver, and lung (but not spleen). These same treated mice also have persistent bacteremia despite a r ..... For more information please see the full descriiption on the strain data sheet
002269	B6.129S6-Cd4^tm1Knw/J	Repository- Live
	Mice homozygous for the Cd4^tm1Knw targeted mutation have a significant block in CD4⁺ T-cell development; 90% of their circulating T-cells are CD8⁺. Homozygous mutant mice also show a Class II restricted deficit in helper T-cell activity and other T-cell responses.
006413	B6.129S6-Erap1^tm1Luc/J	Repository- Live
	Homozygous mutant mice are viable and fertile. The absence of mRNA in splenocyte and of protein in hepatocyte lysates is confirmed via RT-PCR and immunoblot, respectively. Homozygous mutants display reduced cell surface expression of MHC class Ia and Ib molecules, altered presentation of self- and foreign-antigens, and defective CD8⁺ T-cell responses against class I-presented antigens. These mutant mice may be useful in immunological studies exploring ERAP1's role in vivo in optimizing peptides for presentation by MHC class I molecules. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
002128	B6.129S7-Itgb2^tm1Bay/J	Repository- Live
	Mice homozygous for the Itgb2^tm1Bay mutation are viable and fertile. Homozygous mutant mice show an increased neutrophil count, and a decreased inflammatory response to peritonitis. Responses to delayed-type hypersensitivity and rejection of transplanted tissue are impaired. PLEASE NOTE: The Itgb2^tm1Bay allele is not a null mutation; it is a hypomorphic mutation which results in the expression of very low levels of Itgb2 protein. This strain serves as a model for the moderate form of human CD18 deficiency.
002289	B6.129S7-Selp^tm1Bay/J	Repository- Live
	Mice homozygous for the Selp^tm1Bay mutation are viable and fertile. Homoyzgous mutant mice show a deficit in leukocyte rolling and delayed neutrophil extravasation in response to intraperitoneal injections of thioglycollate. Neutrophil count is elevated (2-3-fold). Circulating lymphocyte and monocyte counts are normal. 60-70% reduction in neutrophil emigration into the peritoneum during Streptococcus pneumoniae-induced peritonitis is reduced 60-70%. It can be used as model for human leukocyte adhesion deficiency I syndrome (characterized by elevated levels of circulating leukocytes and impaired leukocyte extravasation to sites of inflammation or infection).
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
001148	B6.AK-H2^k/FlaEgJ	Repository- Live

007227	B6.B10ScN-Tlr4^lps-del/JthJ	Repository- Live
	This spontaneous mutation is a 7 kb deletion in the Tlr4 gene, which results in absence of both mRNA and protein and thus exhibits a defective response to LPS stimulation. The functionally similar Tlr4^Lps-d mutation found in C3H/HeJ mice is a point mutation that causes an amino acid substitution. The allele for normal LPS response, Tlr4^lps-n, occurs in most other C3H and C57BL/10 substrains and most mouse strains. This strain may be used to study the Toll signalling pathway and susceptibility to Gram-negative bacterial infection.
003625	B6.C-H2-Ab1^bm12/KhEg-Mc1r^e-J/J	Repository- Live

000359	B6.C-H2^d/bByJ	Repository- Live

005085	B6.Cg-Cd44^tm1Hbg/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected. Although lymphocyte development appears unremarkable, irregularities are observed in lymphocyte trafficking. Tail-injected lymphocytes derived from null animals exhibit an impaired ability to traffic to peripheral lymph nodes, and to a much greater degree, the thymus. Transcription and translation of the targeted allele subsequently lead to the synthesis of the lacZ protein under control of the 5' regulatory elements of the endogenous locus in all cells and tissues normally expressing one or several of the CD44 isoforms. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary f ..... For more information please see the full descriiption on the strain data sheet
007958	B6.Cg-H2^b3/FlaCmwJ	Repository- Live
	The Qa2, or Ped, complex includes four similar genes and is correlated with the rate of preimplantation embryo development. Qa2^positive mice are characterized by the fast Ped phenotype; Qa2^negative mice, which do not express the QA2 antigen, are characterized by the slow Ped phenotype. This strain, commonly known as B6.K1, is slow Ped or Qa2^negative. B6.K1 females have longer gestation times and smaller litter sizes than the control B6.K2 (Stock No. 007959) females. (Warner CM, 1993) At birth, B6.K1 pups are slighter lighter than B6.K2 pups, but they exhibit an accelerated growth, and by week 6 both male and female B6.K1 mice are significantly heavier than B6.K2 mice. (Watkins A, 2006) At 21 weeks of age, B6.K1 females exhibit elevated systolic blood pressure, and both sexes exhibit elevated serum angiotensin-converting enzyme (ACE) activity. (Watkin ..... For more information please see the full descriiption on the strain data sheet
007959	B6.Cg-H2^b4/FlaCmwJ	Repository- Live
	The Qa2 or Ped complex includes four similar genes. The functional (Qa2^positive) and null (Qa2^negative) alleles correlate with the rate of preimplantation embryo development such that Qa2^positive mice are characterized by the fast Ped phenotype and Qa2^negative mice, which do not express the QA2 antigen, are characterized by the slow Ped phenotype. This strain, commonly known as B6.K2, is fast Ped or Qa2^positive. B6.K2 mice were developed to provide a control for B6.K1 mice (Stock No. 007958). (Warner CM, 1993; Watkins A, 2006)
001317	B6.Cg-Igh^a Thy1^a Gpi1^a/J	Repository- Live
	This congenic strain was made by mating together, not backcrossing, three individual congenic strains carrying differential alleles already on a C57BL/6J genetic background (B6.C-Igh^a, B6.PL-Thy1^a, and B6.CAST-Gpi1^a). This triple congenic is useful as a cellular marker in transplantation studies in conjunction with C57BL/6J inbred mice (Igh^b, Thy1^b, Gpi1^b). Igh is a B cell specific marker, Thy1 is a T cell specific surface marker, and Gpi1 is an enzyme that is widely expressed in mouse tissues, cultured fibroblasts, and in several types of tumors.
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.
005023	B6.Cg-Thy1^a/Cy Tg(TcraTcrb)8Rest/J	Repository- Live
	This transgenic strain carries a rearranged T cell receptor transgene specific for the mouse homologue (pmel-17) of human SILV (gp100), an enzyme involved in pigment synthesis that is expressed by the majority of malignant melanoma cells including B16 melanoma, as well as by normal melanocytes. The strain is also homozygous for the T lymphocyte specific Thy1^a (Thy1.1) allele. CD8+ T cells express a Tcra-V1/Tcrb-V13- transgenic TCR that recognizes an epitope of pmel-17 corresponding to amino acids 25-33 of gp100 presented by H2-D^b MHC class I molecules. Greater than 95% of the CD8+ T cells in transgenic mice expressed the transgenic TCR based on the expression of Vbeta13, amounting to about 20% of all splenocytes. T cells in blood and spleen generally expressed baseline levels of the activation/effector markers CD25, CD44, and CD69, indicating that most of the transgenic cells were in the naive state. These transgenic mice in conjunction with the poor ..... For more information please see the full descriiption on the strain data sheet
004191	B6.Cg-Tg(HLA-A/H2-D)2Enge/J	Repository- Live
	Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express an interspecies hybrid class I MHC gene, AAD, which contains the alpha-1 and alpha-2 domains of the human HLA-A2.1 gene and the alpha-3 transmembrane and cytoplasmic domains of the mouse H-2D^d gene, under the direction of the human HLA-A2.1 promoter. Immunodetection of the HLA-A2.1 recombinant transgene established that expression was at equivalent levels to endogenous mouse class I molecules. The mouse alpha-3 domain expression enhances the immune response in this system. Compared to unmodified HLA-A2.1, the chimeric HLA-A2.1/H2-D^d MHC Class I molecule mediates efficient positive selection of mouse T cells to provide a more complete T cell repertoire capable of recognizing peptides presented by HLA-A2.1 Class I molecules. The peptide epitopes presented and recognized by mouse T cells in the ..... For more information please see the full descriiption on the strain data sheet
003300	B6.NOD-(D17Mit21-D17Mit10)/LtJ	Repository- Live
	This strain is congenic for a 19 cM segment of Chr 17 extending from D17Mit21 through D17Mit10 that includes the major histocompatibility complex, H2, and the insulin dependent diabetes susceptibility locus Idd1. The name given this segment in the primary reference is c17. Upon histologic examination of the pancreas, a significantly higher percentage of B6.NOD-(D17Mit21-D17Mit10) congenic mice than of C57BL/6J control mice were found to exhibit periinsulitis, and more extensive mononuclear cell infiltrates were observed in the pancreata of these mice. The pancreatic infiltrates were not associated specifically with the islets. Insulitis (intraislet infiltration) was extremely rare, and no more than one affected islet was observed in a single animal, even in cases where extensive perivascular/periductal infiltrates existed. Male and female B6.NOD-(D17Mit21-D17Mit10) mice exhibited similar incidence of pancreatic infiltration; in contrast, female ..... For more information please see the full descriiption on the strain data sheet
005217	B6;129S1-Tlr3^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. Northern blot analysis detects a truncated gene product (mRNA), which is not functional. Unlike wildtype macrophages, macrophages derived from these animals fail to produce inflammatory cytokines, IFN-alpha or IFN-beta when challenged with poly(I:C), polyinosine-polycytidylic acid, a synthetic dsRNA analog. Splenocytes isolated from homozygotes do not respond to viral dsRNA and have diminished IL-6 production. Mice homozygous for the mutation are resistant to poly(I:C) induced shock and produce lower levels of IL-12. This mutant mouse strain may be useful in studies of the toll-like receptor pathway of innate immune response.
003374	B6;129S2-H2^dlAb1-Ea/J	Repository- Live
	Mice that are homozygous null for MHC class II genes H2-Ab1, H2-Aa, H2-Eb1, H2-Eb2, H2-Ea are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. MHC class II gene products (mRNA or protein) are not detected. A dramatic decrease is observed in the number of CD4 positive T cells in thymus, spleen and lymph nodes. This strain should serve as a suitable recipient of xenogenic Class II MHC transgenes allowing the engineering of mouse models of human MHC Class II-associated diseases.
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).
002848	B6;129S4-Fcgr2b^tm1Ttk/J	Repository- Live
	Mice homozygous for the Fcgr2^tm1Ttk targeted mutation are viable and fertile. Myeloid and lymphoid development is normal. Immunoglobulin levels are elevated in response to thymus-dependent and thymus-independent antigens. Mice are sensitive to IgG-triggered degranulation and have an enhanced passive cutaneous analphylaxis reaction.
001165	BALB/c-H2^dm2/KhEgJ	Repository- Live

008332	C.129S1-Igh^tm1Janz/J	Repository- Live
	These mutant mice carry a His₆-tagged Myc gene (cDNA) sequence inserted in the endogenous immunoglobulin heavy chain complex (Igh) locus, which mimics the human endemic Burkitt lymphoma t(8;14)(q24;q32) translocation and mouse plasmacytoma T(12;15) translocation. The His₆-tagged Myc is overexpressed in B-cells throughout B-cell development, as detected by FACS analysis. Tumor-free heterozygotes, 4 to 6 months of age, on a mixed B6;129X1 background, exhibit increased B-cell proliferation and apoptosis and have enlarged lymph nodes and spleen due to follicular hyperplasia. 68% of mutant mice between 6 and 21 months of age develop mature B-cell tumors that are IgM and BCL6 positive. Approximately half of the tumors detected are lymphoblastic B-cell lymphomas that are Burkitt-like in appearance and one fifth as plasmacytomas. The plasmacytomas occur in gut-associated lymphoid tissue (GALT), especially in the mesenteric lymph node and Peyer's ..... For more information please see the full descriiption on the strain data sheet
003814	C.129S2-Cd1^tm1Gru/J	Repository- Live
	Mice homozygous for the Cd1^tm1Gru targeted mutation are deficient in both the Cd1d1 and Cd1d2 genes (CD1.1, CD1.2). Homozygous mutant mice lack the normal natural killer cell -like T cell subset. However, type 2 T helper cell (TH2) response is normal, demonstrating that this T cell subset is not required for TH2 response, as previously believed. 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.
001952	C.B10-H2^b/LilMcdJ	Repository- Live

001107	C.BKa-Igh^b/IcrSmnJ	Repository- Live
	C.BKa-Igh ^b/IcrSmn mice express the immunoglobulin heavy-chain repertoire (Igh^b) of C57BL/Ka. This is a congenic strain arising from a backcross of BALB/cxC57BL/Ka-Igh ^a/Igh ^b to BALB/c from which progeny were intercrossed to obtain mice homozygous for Igh ^b. Initial reports indicated that these mice occasionally expressed IgG2a, but this phenomenon was transient and unpredictable. The C.BKa-Igh ^b/IcrSmn (commonly referred to as C.B-17) is the background strain in which the Prkdc ^scid mutation arose. It is primarily used as a coisogenic control strain for C.B17/Icr-scid. Characteristics of C.BKa-Igh ^b/IcrSmn are essentially those of BALB/c.
001951	C.C3-H2^k/LilMcdJ	Repository- Live

004126	C.Cg-Cd19^tm1(cre)Cgn Igh^b/J	Repository- Live
	The Cd19 promoter specifically directs expression at the earliest stages and throughout B-lymphocyte development and differentiation. A Cre cassette is inserted into the Cd19 exon 2, functionally disrupting the gene. Homozygous mice are Cd19-deficient, whereas heterozygous mice are phenotypically normal and can be used for specific deletion of floxed targets in B-lymphocytes. Mice that are homozygous deficient for Cd19 are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. A deficiency in the B-1 subset of B-lymphocytes is observed along with a concomitant reduction in serum IgM. Homozygous mice are severely impaired in their ability to respond to T-cell-dependent antigens and fail to form splenic germinal centers.
003752	C57BL/10ScNJ	Repository- Live
	The breeder pair of C57BL/10ScN mice, obtained from NIH, that were the progenitors of all mice of this strain at The Jackson Laboratory were tested by PCR analysis for the spontaneous Il12rb2 mutation described by Poltorak et al. (J. Immunol. 167:2106-2111, 2001) and found to carry only the wild type Il12rb2 allele. C57BL/10ScN mice have a deletion of the Tlr4 gene that results in absence of both mRNA and protein and thus in defective response to LPS stimulation. Tlr4^lps-del differs from the Tlr4^Lps-d mutation of C3H/HeJ mice, a point mutation that causes an amino acid substitution. The allele for normal LPS response, Tlr4^lps-n, occurs in most other C3H and C57BL/10 substrains and most other mouse strains.
005145	C57BL/6-Tg(CAG-OVA)916Jen/J	Repository- Live
	Mice that are hemizygous for the transgene are viable, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express the membrane bound chicken ovalbumin OVA gene under the direction of the chicken beta actin promoter coupled with the cytomegalovirus (CMV) immediate-early enhancer. Chicken ovalbumin expression is detected by immunohistochemical analysis of all tissues. Splenocytes from transgenic mice display the 254-267-K^b complex, which is recognized by T-cells from the transgenic strain C57BL/6-Tg(TcraTcrb)1100Mjb/J (Stock No. 3831) and the 323-339-I-A^b complex, which is recognized by T-cells from the transgenic C57BL/6-Tg(TcraTcrb)425Cbn/J (Stock No. 4194). Skin grafts from transgenic mice are rejected by C57BL/6 recipients. Ovalbumin antigen specific T cells can be tracked in vivo. This mutant mouse strain represents a model that may be useful in studies of adoptive transfer and graft rejection a ..... For more information please see the full descriiption on the strain data sheet
002595	C57BL/6-Tg(IghelMD4)4Ccg/J	Repository- Live
	Cells from mice carrying the IghelMD4 transgene recognize hen egg lysozyme. More than 90% of B-cells in the spleen are derived from the transgene (a allotype) and are predominantly IgM and IgD. This strain may be used to study B-cell selection.
005432	C57BL/6-Tg(Ins2-OVA)307Wehi/WehiJ	Repository- Live
	Immunohistochemistry does not detect ovalbumin in the islet beta cells of the pancreas. The double transgenic resulting from a cross of this transgenic stock with C57BL/6-Tg(Tcra Tcrb)1100MjbJ (OT-1) exhibit early onset of spontaneous diabetes with islet infiltration; implying that the beta cells express OVA. One of 60 irradiated Tg(Ins2-OV)307 mice receiving a 1:4 mixture (OT-1 transgenic mice:C57BL/6-Thy1.1 congenic) of bone marrow become diabetic when followed for 10 weeks post transfer. Histolocigal evaluation indicates 22% of the islets are mildly infiltrated 15-21 weeks post transfer. This stock only exhibits antigen presentation in the draining lymph node when the pancreatic islets have been damaged. This ovalbumin expressing model is a tool for assessing antigen ignorance and is used in tumor immunity studies and tissue damage studies.
005433	C57BL/6-Tg(Ins2-OVA)59Wehi/WehiJ	Repository- Live
	Transgenic mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The pancreatic islets exhibit weak ovalbumin- (OV-) specific immunohistologic staining and OV is detectable in the islets by Western blot analysis. These mice develop diabetes following adoptive transfer of activated, but not naive, CD8⁺ T lymphocytes from mice bearing Tg(TcraTcrb)1100Mjb (OT-1). Both CD8⁺ T-cells and CD4⁺ T cells from these transgenic animals are tolerant to ovalbumin. This model provides a tool for assessing the requirements of peripheral T-cell deletion.
005431	C57BL/6-Tg(Ins2-TFRC/OVA)296Wehi/WehiJ	Repository- Live
	Ins2-TFRC/OVA (commonly referred to as RIP-mOVA) line 296-1B hemizygote transgenic mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Immunohistochemical analysis detects strong expression in pancreatic beta cells and kidney proximal tubular cells and weak expression in testes. When C57BL/6-Tg(Ins2-TFRC/OVA)296Wehi/WehiJ is mated to C57BL/6-Tg(TcraTcrb)1100Mjb/J (commonly referred to as OT-1 and recognizes OVA specific T-cells, Stock No. 003831) thymic deletion of OT-1 cells is observed in double transgenic mice, suggesting very low levels of thymic expression. OVA specific CD-8+ T-cells activated by cross presentation infiltrate the pancreas causing beta cell destruction resulting in diabetes. However, these cells do not infiltrate the kidney. Proliferating OT-1 T-cells appeared specifically in the lymph nodes draining the pancreas (PLN's) and kidney (RLN's) on day ..... For more information please see the full descriiption on the strain data sheet
006912	C57BL/6-Tg(Tcra2D2,Tcrb2D2)1Kuch/J	Repository- Live
	Mice hemizygous for this "2D2 TCR" (or MOG 35-55 specific TCR) transgene are viable and fertile. The myelin oligodendrocyte glycoprotein (MOG)-specific transgenic T cells are not deleted nor tolerized and are functionally competent. The majority of thymocytes in 2D2 TCR mice express high and intermediate levels of the transgenic T cell receptor (TCR), indicating efficient positive selection of transgenic T cells. The majority of CD4⁺ splenocytes express the transgenic TCR (as defined by Valpha3.2 and Vbeta11 expression). Cultured splenocytes are responsive to whole myelin oligodendrocyte glycoprotein (MOG) and to MOG 35-55 peptide, but not to ovalbumin (OVA) control peptides. From between 2.5 to 5 months of age, 4% of 2D2 TCR mice develop spontaneous experimental autoimmune encephalomyelitis (EAE), while within the first year 40% of 2D2 TCR mice develop spontaneous, isolated optic neuritis with neither clinical nor histological evidence of EAE. Standard EAE induction protoco ..... For more information please see the full descriiption on the strain data sheet
007567	C57BL/6J-Tg(Itgax-cre,-EGFP)4097Ach/J	Repository- Live
	Mice hemizygous for this CD11c-Cre-GFP transgene are viable and fertile. The CD11c (Itgax) promoter directs bicistronic Cre and EGFP protein expression to dendritic cells (DCs). Expression of EGFP is expected to have equimolar expression with Cre recombinase. When bred with any mouse containing a loxP-flanked sequence of interest, the resulting offspring can have Cre-mediated recombination of the flanked sequence. These CD11c-Cre-GFP transgenic mice (as well as CD11c-Cre transgenic mice (see Stock No. 008068)) may be useful for immunological studies utilizing Cre-lox technology or fluorescent protein expression in dendritic cells.
002962	C;129S-Cd1^tm1Gru/J	Repository- Live
	Mice homozygous for the Cd1^tm1Gru targeted mutation are deficient in both the Cd1d1 and Cd1d2 genes (CD1.1, CD1.2). Homozygous mutant mice lack the normal natural killer cell-like T cell subset. However, type 2 T helper cell (TH2) response is normal, demonstrating that this T cell subset is not required for TH2 response, as previously believed.
008312	CBy.129P2(B6)-Tcrd^tm1Mom/SzJ	Repository- Live
	Mice homozygous for the Tcrd^tm1Mom targeted mutation are viable and fertile. Gamma delta T-cell receptor expression is deficient in all adult lymphoid and epithelial organs. There is normal development of the alpha beta T-cell lineage. Patterns of CD4⁺CD8^- and CD4^-CD8⁺ alpha beta T-cells are apparently normal. Mice do not develop inflammatory bowel disease. 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.
006483	CBy.129S2(B6)-Cd4^tm1Mak/J	Repository- Live
	Mice homozygous for the Cd4^tm1Mak targeted mutation have a significant block in CD4⁺ T-cell development; 90% of their circulating T-cells are CD8⁺. Cell surface expression of CD4 protein is not detected on thymocytes and lymph node cells from homozygous mice. Homozygous mutant mice also show a Class II restricted deficit in helper T-cell activity and other T-cell responses. This mutant mouse strain may be useful in studies of T cell development, susceptibility to viral infection and inflammation. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. 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.
005307	CBy.Cg-Thy1^a Tg(TcraCl4,TcrbCl4)1Shrm/ShrmJ	Repository- Live
	Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities.The TCR expressed from this transgene is specific for influenza virus A/PR/8 hemagglutinin (HA) in the context of the MHC class I moleculeH2-K^d. Both thymic and peripheral T-cell populations are skewed toward CD8+ cells. The majority of thymocytes and virtually all CD8⁺ T cells in lymph nodes express the transgenic TCR beta chain. About 40% of peripheral blood CD8⁺ T cells react with the HA peptide presented by H2-K^d. When mated with Tg(Ins2-HA)165Bri, double transgenic neonates have similar levels of V-beta 8 and total number of thymocytes as Tg(TcraCl4,TcrbCl4) mice however the double transgenics become spontaneously diabetic after birth and die within 10 days. This mouse is further modified with the Thy1.1 allele, rather than the alternate allele present in C57BL/10, DBA/2, and BALB/c mice. T ..... For more information please see the full descriiption on the strain data sheet
005443	CBy.PL(B6)-Thy1^a/ScrJ	Repository- Live
	This BALB congenic strain carries the T lymphocyte specific Thy1^a (Thy1.1) allele. Donor T cells can be distinguished from recipient T cells by both flow cytometry and histological analysis.
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
006611	NOD.129P2(B6)-B2m^tm1Unc Tg(HLA-A/H2-D/B2M)1Dvs/DvsJ	Repository- Live
	NOD mice carrying only the HLA-A/H2-D/B2M transgene, commonly referred to as NOD.HHD, (Stock No. 006604) develop significantly accelerated diabetes onset compared to NOD/ShiLtDvs (NOD) inbred mice. This mutant stock is also homozygous for the B2m^tm1Unc mutation which normally prevents the development of of CD8⁺ T cells. The presence of the transgene in the B2m-deficient background, however, restores CD8⁺ T cells, but at a significantly lower level than in NOD inbred mice. Due to the covalently linked nature of the B2M component encoded into the transgene, the transgenic construct is unable to rescue murine MHC class 1 molecules in the NOD.B2m deficient (Stock No. 002309) mice. Thus, these double mutant mice only express human HLA-A2.1. Fifty-five percent of these NOD transgenic B2m-deficient mice develop diabetes b ..... For more information please see the full descriiption on the strain data sheet
008224	NOD.129S2(B6)-Cd74^tm1Doi/LwnJ	Repository- Live
	Mice homozygous for the Cd74 targeted mutation are viable and fertile. Cd74 deficiency affects CD4 T cell development; therefore these mice have very few CD4⁺ T cells. Antigen presenting cells have reduced, though not abolished, ability to present MHC class II antigens, such as GAD. These mice are protected from diabetes. This stock is important for investigation of MHC class II molecule associated self-antigen selection and the importance of self-peptide in CD4 T cell selection and development.
002591	NOD.B10Sn-H2^b/J	Repository- Live
	This congenic strain serves as a diabetes-resistant control for comparison to the NOD/LtJ strain (Stock No. 001976). The diabetes resistant MHC H2^b haplotype was transferred from C57BL/10J mice to the NOD/Lt strain. These mice exhibit some but not all of the immune dysfunctions of NOD/LtJ mice. They are useful in dissecting the role of MHC versus non-MHC genes in producing aberrant immunophenotypes.
006809	NOD.B6-(D11Nds1-D11Mit41)/J	Repository- Live
	Chromosome 11 congenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. The reported conclusion of diabetes resistance in this Chr 11 congenic has been re-evaluated now that the B6 contaminating genome on Chr 1 has been eliminated. Diabetes incidence studies preformed at The Jackson Laboratory show an accelerated onset and incidence of diabetes in females when compared with NOD/ShiLtJ controls and the original stock 005311, while the diabetes onset and incidence in males is accelerated compared to the original Stock 005311 and is slightly reduced compared to NOD/ShiLtJ controls. 006809 incidence study and fine mapping data. 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 characterize ..... For more information please see the full descriiption on the strain data sheet
006935	NOD.Cg-H2^b thnh/J	Repository- Live
	Thin hair homozygotes have a sparse coat discernible by two weeks of age. By three weeks of age the pelt has fewer zigzag hairs than normal and by four weeks of age skin follicles are somewhat dilated with degeneration of the deepest portions of the anagen hair follicles. Hair fragments from degenerating follicles are found in the connective tissue and granulomatous inflammation develops.
006608	NOD.Cg-Igh-6^tm1Cgn Tg(IghelMD4)4Ccg/DvsJ	Repository- Live
	NOD.Cg-Igh-6^tm1Cgn Tg(IghelMD4)4Ccg/DvsJ (NOD.IgHEL Igh-6-deficient) mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Because these mice are Igh-6-deficient, they do not express endogenous IgM. All B lymphocytes in NOD.IgHEL Igh-6-deficient mice express Ig molecules specific for hen egg lyzozyme (HEL). There is no significant difference in the total number of B and T lymphocytes between NOD.IgHEL Igh-6-deficient and NOD.IgHEL (Stock No. 006345) mice. The incidence of diabetes in transgenic vs. non-transgenic NOD.Igh-6-deficient mice is similar by 21 weeks of age, (16.7% vs. 13.6%, respectively). Histological evaluation of 12 week old NOD.IgHEL Igh-6-deficient mice shows that most mice have low levels of insulitis compared to NOD/ShiLt control mice, although an occasional animal had extensive insulitis. In ..... For more information please see the full descriiption on the strain data sheet
006605	NOD.Cg-Prkdc^scid Emv30^b Tg(HLA-A/H2-D/B2M)1Dvs/DvsJ	Repository- Live
	Although NOD mice that carry this transgene (Stock No. 006604) develop diabetes significantly earlier than do NOD/ShiLtDvs (NOD) controls, this transgenic strain harbors the Prkdc^scid mutation (characterized by an absence of functional T cells and B cells), and therefore does not become diabetic. This strain is useful for adoptive transfer experiments, and as a source of insulitis free pancreatic islets.
004460	NOD.Cg-Tg(TcraBDC2.5)1Doi Tg(TcrbBDC2.5)2Doi/DoiJ	Repository- Live
	NOD.Cg-Tg(TcraBDC2.5)1Doi Tg(TcrbBDC2.5)2Doi/DoiJ mice carry both rearranged TCR alpha and beta genes from the cytotoxic CD4+ T cell clone BDC-2.5. When paired with a homozygous Rag1^tm1Mom mutation (such as in Stock No. 003729), recombination of endogenous TCR and Ig is prevented so that mature T cells in these mice express only the BDC2.5 TCR. On the NOD background, mice carrying the transgenes have a reduced incidence of diabetes relative to NOD/ShiLtJ controls (12% incidence at age 30 weeks). When coupled with the homozygous Rag1^tm1Mom mutation, mice develop diabetes extremely early (mean age of 25 days). (Katz et al 1993, Gonzalez et al 2001, Mombaerts et al 1992)
005868	NOD.Cg-Tg(TcraTcrbNY8.3)1Pesa/DvsJ	Repository- Live
	NOD.Cg-Tg(TcraTcrbNY8.3)1Pesa/DvsJ, commonly called 8.3-NOD, express rearranged Tcra and Tcrb transgenes derived from the pancreatic beta cell-cytotoxic CD8⁺ T cell clone NY8.3. CD4^-CD8⁺ thymocytes and lymph derived T cells are skewed toward VB8.1/2⁺ expression when compared to wild type controls. Although, transgenic mice exhibit dramatically accelerated diabetes, the cumulative diabetes incidence and kinetics of disease are remarkably similar to their wild type cohorts. Insulitis scores of 3 week old transgene⁺ mice was significantly lower, while insulitis scores of 6 week olds were significantly more severe than in wild types controls, Verdaguer J et al, 1997, J. Exp Med 186, 1663-1676. Transgenic animals bearing both TCR transgenes offer a source of CTL precursors useful in examining the diversity of beta cell peptides recognized by the autoreactive CD8⁺ T lymphocytes contributing to th ..... For more information please see the full descriiption on the strain data sheet
004483	NOD.NON-Thy1^a/1LtJ	Repository- Live

002032	NOD.SW-H2^q/J	Repository- Live
	This congenic strain carries the diabetes-resistant MHC from the from SWR/J (Stock No. 000689) and is used as a comparison to the NOD/ShiLtJ (Stock No. 001976). These mice exhibit some but not all of the immune dysfunctions of NOD/ShiLtJ mice. These mice are useful for dissecting the role of MHC versus non-MHC genes in producing aberrant immunophenotypes.
005328	NOD/ShiLt-Tg(Cd4-DsRed)4Lt/J	Repository- Live
	The donating investigator reports that hemizygous transgenic mice are viable, fertile and normal in size. FACS analysis of splenic lymphocytes shows transgenic expression in 36% of CD4⁺ and 6% of CD8⁺ T-cells and minimal expression (background levels) in B cells and macrophages. When compared to wild-type NOD/ShiLt mice, the diabetes incidence is lower (50%) and diabetes onset is delayed. Adoptive transfer experiments with splenocytes and bone marrow from hemizygous CD4-DsRed transgenic mice does not confer diabetes protection on NOD inbred mice, suggesting that the agent of protection is not dependent on hematopoietic cells. No homozygous transgenic mice have been identified in litters produced from hemizygote intercrosses, suggesting that homozygotes are not viable. This strain is useful for tracking resting and activated T cells in vivo and in vitro.
005334	NOD/ShiLt-Tg(Cd4-EGFP)1Lt/J	Repository- Live
	Homozygous transgenic mice are viable, fertile, normal in size and do not exhibit any gross physical or behavioral abnormalities. The donating investigator reports uniform transgenic expression, about 81% of inactivated or resting CD8⁺ T cells and CD4⁺ T cells, with minimal expression in B cells (2.3%) and macrophages (1.5%). Over a three day period following activation in vitro with anti-CD3, gating on live populations of CD4⁺ and CD8⁺ subsets show continued GFP expression in both. However, there is a greater diminution of GFP fluorescence in the activated CD8⁺ T population by day three in vitro. Diabetes onset is similar to wild-type NOD/ShiLt mice. These CD4-GFP transgenic mice may be useful for fluorescent monitoring of T cells both in vivo and in vitro.
006604	NOD/ShiLtDvs-Tg(HLA-A/H2-D/B2M)1Dvs/J	Repository- Live
	This transgenic NOD mouse model, commonly referred to as NOD.HHD, develops significantly accelerated diabetes onset compared to NOD/ShiLtDvs (NOD) inbred mice. When transgenic mice are bred to NOD-B2m-deficient mice (e.g. Stock No. 002309), which completely lack CD8⁺ T cells, CD8⁺ T cells are restored in the double mutant mice, but at significantly lower levels than in NOD inbred mice. FACS analysis indicates that the transgenic NOD-B2m-deficient mice express only the HLA-A2.1/H2-D^b chimeric class I molecule. In contrast to NOD.B2m^tm1Unc females, which are diabetes free, 55% of the transgenic NOD B2m-deficient females develop diabetes by 30 weeks of age. Insulitis scores determined by histological examination are similar between the NOD double mutant mice and NOD/ShiLtDvs inbred mice, and cultured pancreatic islets from transgenic NOD B2m-deficient mice an ..... For more information please see the full descriiption on the strain data sheet
003899	STOCK Cd44^tm1Hbg/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected. Although lymphocyte development appears unremarkable, irregularities are observed in lymphocyte trafficking. Tail-injected lymphocytes derived from null animals exhibit an impaired ability to traffic to peripheral lymph nodes, and to a much greater degree, the thymus. Transcription and translation of the targeted allele subsequently lead to the synthesis of the lacZ protein under control of the 5' regulatory elements of the endogenous locus in all cells and tissues normally expressing one or several of the CD44 isoforms.
002397	129-Cd5^tm1Cgn/J	Repository-Cryopreserved
	Mice homozygous for the Cd5^tm1Cgn targeted mutation are viable and apparently healthy. Both T and B cells in homozygous mutant mice lack surface CD5. Mice show normal immune responses to both T cell-dependent and -independent antigens.
002399	129-Igh-5^tm1Cgn/J	Repository-Cryopreserved
	Mice homozygous for the Igh-5^tm1Cgn targeted mutation are viable and fertile. Homozygous mutant mice show a delay in affinity maturation although they are able to generate high affinity B cell memory. Heterozygous mice show a disproportionate percentage of B cells expressing the wildtype IgH allele. Also known as IgD.
007172	129S6.129X1(B6)-Ptprc^tm1Weis/J	Repository-Cryopreserved
	Mice homozygous for this targeted point mutation are viable and fertile. The phenotype of this mutation, which inactivates the inhibitory wedge of the protein, is dependent upon the genetic background. On the 129S6 background, B, T, and myeloid cells are hyperresponsive to stimulation at a biochemical and cellular level. B cell development is skewed to the B1 cell lineage. A mild lymphoproliferative disorder develops, but the autoantibodies associated with the mixed C57BL/6 and 129 background do not (or do so at low titer). Cell surface expression of the protein is indistinguishable from wildtype as determined by flow cytometry of hematpoietic lineages in bone marrow, lymph node, spleen, thymus, peritoneal lavage, and peripheral blood.
000472	A.CA-H2^f H2-T18^a/SnJ	Repository-Cryopreserved

001066	A.TH-H2^t2/SfDvEgMobJ	Repository-Cryopreserved

001067	A.TL-H2^t1/SfDvEgMobJ	Repository-Cryopreserved

002089	AK.B6-H2^b Fv1^b/J	Repository-Cryopreserved

002090	AK.B6-H2^b/J	Repository-Cryopreserved

001094	AK.L-H2^b/1CyTyJ	Repository-Cryopreserved

001095	AK.L-H2^oz2/CyJ	Repository-Cryopreserved

001096	AK.L-H2^oz3/CyJ	Repository-Cryopreserved

001027	AK.L-Igh-1a^a/CyTyJ	Repository-Cryopreserved

000470	AK.M-H2^m H2-T18^a/nSnJ	Repository-Cryopreserved

003851	ALR.NOD-(D17Mit30-D17Mit123)/Lt	Repository-Cryopreserved
	This congenic strain carries the H2 major histocompatibility complex from NOD/Lt on a background that is otherwise, statistically, 99.9% of ALR/Lt origin. The introgessed chromosomal segment from NOD/Lt in this strain, previously called ALR.NOD-H2^g7, has been defined by microsatellite analysis and the strain renamed accordingly. The most proximal marker identified within the NOD-derived segment is D17Mit30, at 16.4 cM just 3.6 cM from the most proximal gene in the H2 complex. The introgressed segment includes all of the H2 complex and extends 33.7 cM distally from it.
000132	B10.129P-H10^b/(9M)SnJ	Repository-Cryopreserved

000416	B10.129P-H11^b/(10M)SnJ	Repository-Cryopreserved

000417	B10.129P-H12^b/(6M)SnJ	Repository-Cryopreserved

000409	B10.129P-H1^b Hbb^d Tyr^c Ea7^a/(5M)oSnJ	Repository-Cryopreserved

000418	B10.129P-H1^b Tyr^c Hbb^d/(5M)nSnJ	Repository-Cryopreserved

000414	B10.129P-H46^b H47^b/(21M)Sn	Repository-Cryopreserved

002447	B10.129S2(B6)-Cd4^tm1Litt/J	Repository-Cryopreserved
	Mice homozygous for the Cd4^tm1 targeted mutation have a significant block in CD4⁺ T-cell development; 90% of their circulating T-cells are CD8⁺. Homozygous mutant mice also show a Class II restricted deficit in helper T-cell activity and other T-cell responses.
001150	B10.A-H2^h4/(4R)SgDvEgJ	Repository-Cryopreserved

001149	B10.A-H2ⁱ³/(3R)SgDvEgJ	Repository-Cryopreserved

000467	B10.A-H2ⁱ⁵ H2-T18^a/(5R)SgSnJ	Repository-Cryopreserved

000466	B10.AKM-H2^m H2-T18^a/SnJ	Repository-Cryopreserved

001954	B10.AQR-H2^y1/KljMcdJ	Repository-Cryopreserved

000432	B10.C-H1^b Hbb^d Tyr^c/(41N)SnJ	Repository-Cryopreserved

000433	B10.C-H3^c H13^? A/(28NX)SnJ	Repository-Cryopreserved

000429	B10.C-H3^c/SnJ	Repository-Cryopreserved

000430	B10.C-H7^b/(47N)SnJ	Repository-Cryopreserved

000431	B10.C-H9^b/(45N)SnJ	Repository-Cryopreserved

000427	B10.CE-H13^b A^w/(30NX)SnJ	Repository-Cryopreserved

005308	B10.Cg-H2^d Tg(TcraCl4,TcrbCl4)1Shrm/ShrmJ	Repository-Cryopreserved
	Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities.The TCR expressed from this transgene is specific for influenza virus A/PR/8 hemagglutinin (HA) in the context of the MHC class I molecule H2-K^d. Both thymic and peripheral T-cell populations are skewed toward CD8+ cells. The majority of thymocytes and virtually all CD8+ T cells in lymph nodes express the transgenic TCR beta chain. About 40% of peripheral blood CD8+ T cells react with the HA peptide presented by H2-K^d. When mated with Tg(Ins2-HA)165Bri, double transgenic neonates have similar levels of V-beta 8 and total number of thymocytes as Tg(TcraCl4,TcrbCl4) mice however the double transgenics become spontaneously diabetic after birth and die within 10 days. This transgenic model is useful in the study of T-cell activation, cross presentation of antigens, process of thymic selection, peripheral tolerance and ..... For more information please see the full descriiption on the strain data sheet
005534	B10.Cg-H2^d Tg(Ins2-HA)165Bri/ShrmJ	Repository-Cryopreserved
	Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities. Mice homozygote for the transgene have silver grey fur color. Hemizygous and wildtype mice are black. Immunohistochemistry reveals pancreatic islet cell expression of the transgene and no expression in the spleen, kidney or thymus. Isolated islets stain normally for insulin and are morphologically indistinguishable from control islets. Additional functional studies found no expression in bone marrow. Histology revealed no insulitis and the single transgenic mice do not become diabetic. T-cell proliferation assays, Cytotoxic Lymphocyte (CTL) assays, and adoptive transfer studies performed using transgenic mice indicate significantly reduced class 1 and class II T-cell responses compared to controls. Hemagglutination inhibition assays of sera from HA primed transgenic mice indicate antibody titers slightly lower but nearly equivalent to HA primed control m ..... 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.
005895	B10.Cg-Thy1^a H2^d Tg(TcraCl1,TcrbCl1)1Shrm/J	Repository-Cryopreserved
	Male mice that are hemizygous for the Clone-1 TCR (also called Clone 1 Thy1.1 TCR or Cl.1 TCR) transgene are viable, fertile, and normal in size. Females are very weak and have low fecundity. The donating investigator reports that all transgenic mice are prone to tumor development by 5-6 months of age. The transgene encodes a rearranged low avidity T cell receptor that recognizes an influenza virus hemagglutinin epitope (HA_518-526) restricted by MHC class I H-2K^d. Flow cytometric analysis shows appropriate skewing towards the CD8⁺ T cell compartment in thymocytes and peripheral lymphocytes. Both naive and activated clone 1 T cells exhibit decreased responsiveness when presented with their cognate antigen in vitro and when transferred into mice expressing HA on pancreatic beta cells. CD8⁺ T cells can be induced to exhibit both effector function and antitumor activity. This mouse is further modified with the Thy1.1 allele, rather than th ..... For more information please see the full descriiption on the strain data sheet
000428	B10.D2-H11^?/(55N)SnJ	Repository-Cryopreserved

000425	B10.D2-H1^a/(58N)SnJ	Repository-Cryopreserved

001163	B10.D2-H2^bm23/EgJ	Repository-Cryopreserved
	The H2^bm23 mutant allele causes an increase in the percentage of the CD8 T cells bearing Valpha3.2 both in peripheral T cells and CD8 single positive thymocytes. (sim et al, 1997.)
000462	B10.D2-H2^d/n2SnJ	Repository-Cryopreserved

001164	B10.D2-H2^dm1/EgJ	Repository-Cryopreserved

001151	B10.D2-H2^g3/(103R)EgJ	Repository-Cryopreserved

001153	B10.D2-H2ⁱ⁷/(107R)EgJ	Repository-Cryopreserved

001152	B10.D2-H2^ia/(106R)EgJ	Repository-Cryopreserved

000426	B10.D2-H8^b/(57N)SnJ	Repository-Cryopreserved

000460	B10.D2-Hc⁰ H2^d H2-T18^c/o2SnJ	Repository-Cryopreserved
	This congenic strain carries the H2^d haplotype from DBA/2J following six generations of backcrossing to C57BL/10Sn. This strain still carries the Hc⁰ allele from DBA/2J, making them serum C5 deficient. Mice have increased susceptibility to certain pathogens and impaired chemotactic responses of neutrophils. Allograft rejection is prolonged. The following inbred strains are also homozygous for the Hc⁰ allele: A/HeJ (Stock No. 000645), AKR/J (Stock No. 000648), DBA/2J (Stock No. 000671), NOD/LtJ (Stock No. 001976), NZB/BlNJ (Stock No. 000684), and SWR/J (Stock No. 000689).
003147	B10.D2-Hc¹ H2^d H2-T18^c/nSnJ-Tg(DO11.10)10Dlo/J	Repository-Cryopreserved
	Clonal deletion of autoreactive T cells in vivo was studied using a peptide antigen to induce deletion of antigen-reactive thymocytes. Mice transgenic for a T cell receptor that reacts to this peptide (Tg(DO11.10)10Loh) contain thymocytes that progress from the immature to the mature phenotype. Intraperitoneal administration of the peptide antigen to transgenic mice results in a rapid deletion of the immature CD4⁺ CD8⁺ TCR^lo thymocytes. Apoptosis of cortical thymocytes can be seen within 20 hours of treatment. These results provide direct evidence for the in vivo role of apoptosis in the development of antigen-induced tolerance.
000464	B10.DA-H2^qp1 H2-T18^b/(80NS)SnJ	Repository-Cryopreserved

001823	B10.F-H2^bp5/(14R)J	Repository-Cryopreserved

001818	B10.F-H2^pb1/(13R)J	Repository-Cryopreserved

001012	B10.HTG-H2^g/2CyJ	Repository-Cryopreserved

000999	B10.HTG-H2^g/3CyJ	Repository-Cryopreserved

000423	B10.KR-H13^? A/SnJ	Repository-Cryopreserved

001894	B10.LG-H2^ar1/J	Repository-Cryopreserved

000420	B10.LP-H13^b A^w/Sn	Repository-Cryopreserved

000422	B10.LP-H3^b H13^b/(36NS)Sn	Repository-Cryopreserved

000421	B10.LP-H3^b/Sn	Repository-Cryopreserved

000459	B10.M-H2^f H2-T18^a^?/SnJ	Repository-Cryopreserved
	This congenic strain carries H2^f derived from the non-inbred stock M (see development field). This strain also carries the Pgk2^b allele and the Tla^d allele. (Snell GD, 1958; Snell GD, 1978; Eicher et al., 1978; Flaherty et al., 1977).
001068	B10.M-H2^f/nMobJ	Repository-Cryopreserved

000739	B10.M-H2^fm2/MobJ	Repository-Cryopreserved

001154	B10.MBR-H2^bq1/SxEgJ	Repository-Cryopreserved

001790	B10.MBR/SxJ	Repository-Cryopreserved

001825	B10.P-H2^kp1/(10R)SgJ	Repository-Cryopreserved

000477	B10.PA-Pldn^pa H3^e a^t/SnJ	Repository-Cryopreserved
	This minor histocompatibility 3 (H3^e) congenic strain is also carrying the closely linked pallid mutation (Pldn^pa) as well as the black and tan allele of nonagouti also residing on Chromosome 2. Histocompatibility 3 is one of several loci isolated and identified by Dr. George Snell and co-workers. Histocompatibility gene differences were identified by generating congenic resistant strains and testing for resistance to transplantable tumors. Homozygous pallid mice have pink eyes, a diluted coat color and their viability is slightly reduced. Some homozygotes have slightly abnormal behavior, with abnormal postural responses and head tilting due to the absence of otoliths in the sacculus and utriculus in many but not all mutant mice. The effect of pallid on behavior and otolith morphology appears to be a result of manganese deficiency. Homozygotes display defective mucopolysaccharide synthesis in the otolith matrix and a slower rate of transport of manga ..... For

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