Search Criteria: Research Area is "Immunology and Inflammation Research: Immunodeficiency (MHC class II defects)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 005977 | B6.129S2(C)-Stat6tm1Gru/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. | ||
| 003239 | B6.129S2-Ciitatm1Ccum/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable and fertile when housed under specific pathogen-free conditions. Mice do not express conventional MHC class II molecules on the surface of splenic B cells and dendritic cells. In addition, interferon gamma stimulated peritoneal macrophages and somatic tissues from homozygous mutant mice do not express MHC class II molecules. The levels of invarient chain and H2m gene transcripts are substantially decreased in class II transactivator deficient mice. Homozygous mice have very few mature CD4 T cells in the periphery despite MHC class II expression in the thymus. | ||
| 004513 | B6.129S2-H2-DMatm1Doi/J | Repository-Cryopreserved |
| 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 (mRNA) is detected in splenocytes by PCR. Homozygous mice express normal numbers of a single major histocompatibility complex class II molecules primarily loaded with a single peptide. APC presentation of whole proteins and short peptides antigens is defective. Although total thymocyte number is normal, the number of CD4+CD8- cells is reduced by 20-50%. This mutant mouse strain may be useful in studies of MHC class II restricted antigen presentation. | ||
| 002729 | B6.129S6-Cd74tm1Liz/J | Repository-Cryopreserved |
| Mice homozygous for the Iitm1Liz targeted mutation are viable and fertile. Ia-associated invariant chain deficient mice have defects in MHC Class II assembly, transport, surface expression, and antigen presentation. Homozygous mutant mice lack mature CD4+ cells. | ||
| 002643 | B6;129S4-H2-DMatm1Luc/J | Repository-Cryopreserved |
| Mice homozygous for the H2-Matm1Luc targeted mutation are viable and fertile but generally smaller than wildtype siblings. Defects in immunological responses in homozygous mutant mice include defects in loading of peptides into the MHC class II molecules, presentation of antigen in a MHC class II restricted manner, and intrathymic T-cell positive and negative selection. This strain may be useful as a model for examination of MHC class II restricted antigen presentation, tissue graft rejection, and T-cell repertoire selection. | ||
| 003238 | C.129S2(B6)-Ciitatm1Ccum/J | Repository-Cryopreserved |
| Mice homozygous for the targeted mutation are viable and fertile when housed under specific pathogen-free conditions. Mice do not express conventional MHC class II molecules on the surface of splenic B cells and dendritic cells. In addition, interferon gamma stimulated peritoneal macrophages and somatic tissues from homozygous mutant mice do not express MHC class II molecules. The levels of invarient chain and H2m gene transcripts are substantially decreased in class II transactivator deficient mice. Homozygous mice have very few mature CD4 T cells in the periphery despite MHC class II expression in the thymus. | ||
| 002730 | CAn.129S6(B6)-Cd74tm1Liz/J | Repository-Cryopreserved |
| Mice homozygous for the Iitm1Liz targeted mutation are viable and fertile. The phenotype exhibited by mutant mice lacking the Ii (Ia-associated invariant chain) gene product is appreciably influenced by genetic background. As expected in BALB/cAn-Iitm1Liz mice, class II surface expression is markedly decreased. However, discordant expression of class II conformational epitopes is not detected, indicating that the few class II molecules present are properly folded and possess a normal configuration. Although spleen cells are ineffective for presentation of intact protein antigens, they show consistently superior peptide-loading capabilities. Thus surface class II molecules appear empty or occupied by easily displaced peptide(s). B lymphocyte development appears defective particularly in lymph node populations. Mature splenic dendritic cells in Ii chain mutants also display reduced class II surface expression. Thymi contain 3-fold fewer CD4+ T lymphocytes, but maturatio
..... For more information please see the full descriiption on the strain data sheet | ||
| 005356 | NOD.129(B6)-B2mtm1Unc Ciitatm1Ccum/BhsJ | Repository-Cryopreserved |
| NOD.129(B6)-B2mtm1UncC2tatm1Ccum/BhsJ is homozygous for linkage markers delineating Idd1-5, 7-10 and 13-15 loci of NOD origin and do not become diabetic. Histology indicates normal islet tissue structure with no cellular infiltration. Islets are intact and produce insulin. FACs analysis of peripheral blood cells of mice homozygote for B2mtm1Unc and C2tatm1Ccum confirmed the absence of MHC I or MHC II cell surface expression, reduced peripheral T-cell populations, deficiency of CD4+ and CD8+ T-cells and there is no difference in B-cell numbers when compared with wild-type controls. Additionally, B2mtm1Unc,C2tatm1Ccum double homozygous animals exhibit lower IgG titers and higher IgM titers than wild-type controls. Diabetic NOD females receiving purified islets from NOD.129(B6)-B2mtm1UncC2tatm1Ccum/BhsJ transplanted under the kidney capsule remain normal
..... For more information please see the full descriiption on the strain data sheet | ||
| 004448 | NOD.129S2(B6)-Ciitatm1Ccum/FlvJ | Repository-Cryopreserved |
| In humans, a non-functional C2ta (or Ciita) gene causes bare lymphocyte syndrome (BLS), which is characterized by the lack of HLA class II gene expression and a reduced number of mature CD4+ T cells in the periphery. On the C57BL/6 congenic background (see Stock No. 003239) disruption of C2ta results in a lack of MHC Class II expression by splenic B cells, dendridic cells, and both resting and interferon gamma stimulated macrophages. However, thymic epithelium retains MHC class II expression. Homozygotes also exhibit a significant decrease in the levels of invariant chain and H-2M gene transcripts. Non-conventional MHC Class II molecules such as H-2O alpha and H-2O beta, are not affected by the disruption of C2ta. Despite the continued expression of MHC Class II molecules on cells of the thymic epithilium, few CD4 positive cells exist in the periphery of homozygotes. (Chang et al 1996) Because of
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| 006023 | NOD.Cg-H2-Ab1tm1Gru Tg(CD4,HLA-DQA1,HLA-DQB1)N8Ell/EllJ | Repository-Cryopreserved |
| This NOD congenic strain contains a targeted H2-Ab1 mutation also carries two transgenes: one expressing human CD4 under the regulation of the mouse Cd4 enhancer and a second expressing human HLA-DQ6. The latter transgene confers dominant protection to development of Type 1 diabetes in humans. These double transgenic, H2-Ab1-deficient mice are viable, fertile, normal in size, and free of both autoimmune diabetes and cardiomyopathy, a phenotype found in an NOD stock expressing an HLA-DQ8 transgene (Elliot JF et al. Proc Natl Acad Sci U S A 2003; 100:13447-52). By 55 weeks of age, 100% of the H2-Ab1-deficient, DQ6 transgenic mice develop thyroiditis and thyroid autoantibodies. Of these, 25% develop thyroid gland enlargement and goiter, and a subset of these animals develops thyroid failure with elevated serum TSH levels.
This model is useful for studying autoimmune thyroid disease and to understand the role of MHC class II in au
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