Analysis Tools
normal phenotype
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• develop normally, are fertile, and do not show any sign of inflammatory bowel disease
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Allele Symbol Allele Name Allele ID |
Il10tm1Roer targeted mutation 1, Axel Roers MGI:3521568 |
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| Summary |
5 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• develop normally, are fertile, and do not show any sign of inflammatory bowel disease
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• increased B cell numbers are observed after immunization with anti-IgD antibody compared to immunized controls
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• plasma cell numbers are 2-fold larger than controls seven days after infection with MCMV
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• are observed after immunization with anti-IgD antibody compared to immunized controls
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• increased myeloid numbers are observed after immunization with anti-IgD antibody compared to immunized controls
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• MCMV-specific CD8 + T cell numbers are about twice as numerous as controls 7 days after infection with MCMV
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• IL-10 levels are half that of wild-type controls when immunized with anti-IgD antibodies
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• IL-10 levels are half that of wild-type controls when immunized with anti-IgD antibodies
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• increased B cell numbers are observed after immunization with anti-IgD antibody compared to immunized controls
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• plasma cell numbers are 2-fold larger than controls seven days after infection with MCMV
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• are observed after immunization with anti-IgD antibody compared to immunized controls
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• increased myeloid numbers are observed after immunization with anti-IgD antibody compared to immunized controls
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• MCMV-specific CD8 + T cell numbers are about twice as numerous as controls 7 days after infection with MCMV
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mutants die by 11th day after T. gondii infection
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• mucosa showed massive hyperplasia and infiltration with inflammatory cells and ectatic lymphatic vessels
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• multifocal mucosal necroses resulted in numerous ulcerations
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• all mutants developed prolapse under standard conditions, 9/15 mutants exhibited prolapse under pathogen free conditions
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• incidence of bowel disease increased with age, reaching 33% at 6 months
• multifocal severe inflammation affected all strata of the colonic wall
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• incidence of bowel disease increased with age, reaching 33% at 6 months
• multifocal severe inflammation affected all strata of the colonic wall
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• expansion of lymph vessels in the intestine
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• displayed a twofold increase in ear thickness after contact with allergen 2,4-dinitrochlorobenzene (DNCB) compared to controls, however innate inflammatory response and response to LPS were normal
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• increased secretion of proinflammatory cytokines, TNF-alpha, IL-6, IL-12 and MCP-1 by stimulated splenocytes
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• severe hepatitis seen after T. gondii infection
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• T. gondii infection resulted in severe hepatitis and death by the 11th day after infection in mutants but not controls
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• severe hepatitis seen after T. gondii infection
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• unlike in vitro, when CD4+ T cells containing Tg(Tcra2D2,Tcrb2D2)1Kuch are transferred into mice they fail to exhibit proliferation
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• mice are resistant to direct and passive MOG-induced experimental autoimmune encephalomyelitis
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• unlike in vitro, when CD4+ T cells containing Tg(Tcra2D2,Tcrb2D2)1Kuch are transferred into mice they fail to exhibit proliferation
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• starting at 10 weeks of age, mice present with the gross manifestations of colitis including colonic thickening and substantial increase in the size of mesenteric lymph nodes
• histological examinations reveals prominent mononuclear infiltration of epithelial tissues as well as tissue destruction of the cecum and portions of the colon
• disease is similar to what is observed in Il10tm1Cgn null mice though with less severity and incidence, and a slightly later onset
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• starting at 10 weeks of age, mice present with the gross manifestations of colitis including colonic thickening and substantial increase in the size of mesenteric lymph nodes
• histological examinations reveals prominent mononuclear infiltration of epithelial tissues as well as tissue destruction of the cecum and portions of the colon
• disease is similar to what is observed in Il10tm1Cgn null mice though with less severity and incidence, and a slightly later onset
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• Foxp3 expressing regulatory CD4 T cells fail to produce IL-10
• mice exhibit spontaneous colitis and inflammation in the lung that is contributable to defective regulatory T cell responses
• mice also have heightened inflammatory responses when challenged with antigen to the lungs or skin
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• there is a substantial increase in ear thickness and inflammation after application of dinitrofluorobenzene (DNFB) on the ear
• T cells infiltrating the site of DNFB application have higher expression of the activation marker CD69
• there is no difference in the number of FoxP3 regulatory T cells found at the site of inflammation when compared to control mice suggesting the inability to make IL-10 is affecting regulator T cell function
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• IL-10 producing T cells are greatly diminished by the Foxp3-expressing, but not Foxp3 negative, CD4+ T cell subset
• there is almost a two-fold reduction in the number of lamina propria Foxp3 negative lymphocytes that produce IL-10
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• mice have mild perivasculitis and moderate mononuclear infiltration around large airways in the lungs
• inducing lung inflammation by sensitizing and then challenging mice with OVA peptide leads to more pronounced inflammatory response with 2.7 fold increase in leukocytes numbers from bronchoalveolar lavage fluid
• OVA induced inflammation leads to markedly increased mucus production, goblet cell expansion, edema, and increased eosinophilic infiltration around major airways
• OVA treated mice also show a marked increase in airway hyperreactivity to aerosolized methacholine
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• mice have mild perivasculitis and moderate mononuclear infiltration around large airways in the lungs
• inducing lung inflammation by sensitizing and then challenging mice with OVA peptide leads to more pronounced inflammatory response with 2.7 fold increase in leukocytes numbers from bronchoalveolar lavage fluid
• OVA induced inflammation leads to markedly increased mucus production, goblet cell expansion, edema, and increased eosinophilic infiltration around major airways
• OVA treated mice also show a marked increase in airway hyperreactivity to aerosolized methacholine
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• Foxp3 expressing regulatory CD4 T cells fail to produce IL-10
• mice exhibit spontaneous colitis and inflammation in the lung that is contributable to defective regulatory T cell responses
• mice also have heightened inflammatory responses when challenged with antigen to the lungs or skin
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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 04/09/2024 MGI 6.23 |
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