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Allele Symbol Allele Name Allele ID |
Cd28tm1Mak targeted mutation 1, Tak Mak MGI:1857150 |
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| Summary |
20 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mutants exhibit weaker cytotoxic T cell responses to influenza virus than wild-type
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• mutants exhibit weaker cytotoxic T cell responses to influenza virus than wild-type
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• few mice (2/13) develop clinical symptoms of EAE following stimulation by myelin oligodendrocyte glycoprotein (MOG) 355-55 peptide
• mice that develop clinical symptoms do so with delayed onset and decreased disease score
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• 50% of mice exhibit inflammatory lesions in meninges and CNS parenchyma as compared to 80% in wild-type following 35 day observation period after EAE induction
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• 50% of mice exhibit inflammatory lesions in meninges and CNS parenchyma as compared to 80% in wild-type following 35 day observation period after EAE induction
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in response to anti-CD3 or anti-CD3 and anti-CD28 antibodies
(J:123989)
• CD4 T cells fail to proliferate in vitro when stimulated with low or high doses of anti-CD3 antibody
(J:130882)
• T cell proliferation fails to respond in a synergistic way to anti-CD3 and anti-CD28 antibodies unlike wild-type cells
(J:205441)
• however, treatment with exogenous IL2 increased proliferation response
(J:205441)
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• slightly
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• isotype switching is impaired compared to in wild-type mice
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• in the thymus and spleen
(J:205441)
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• regulatory T cells from tamoxifen-treated mice exhibit reduced suppression function compared with control cells
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• production from T cell fails to respond in a synergistic way to anti-CD3 and anti-CD28 antibodies unlike wild-type cells
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• CD4 T cells fail to secrete IL-2 upon stimulation with anti -CD3 or -CD3/-CD28 antibodies
(J:130882)
• production from T cell fails to respond in a synergistic way to anti-CD3 and anti-CD28 antibodies unlike wild-type cells
(J:205441)
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• in response to anti-CD3 or anti-CD3 and anti-CD28 antibodies
(J:123989)
• CD4 T cells fail to proliferate in vitro when stimulated with low or high doses of anti-CD3 antibody
(J:130882)
• T cell proliferation fails to respond in a synergistic way to anti-CD3 and anti-CD28 antibodies unlike wild-type cells
(J:205441)
• however, treatment with exogenous IL2 increased proliferation response
(J:205441)
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• slightly
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• isotype switching is impaired compared to in wild-type mice
|
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• in the thymus and spleen
(J:205441)
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• regulatory T cells from tamoxifen-treated mice exhibit reduced suppression function compared with control cells
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• slightly
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• in response to anti-CD3 or anti-CD3 and anti-CD28 antibodies
(J:123989)
• CD4 T cells fail to proliferate in vitro when stimulated with low or high doses of anti-CD3 antibody
(J:130882)
• T cell proliferation fails to respond in a synergistic way to anti-CD3 and anti-CD28 antibodies unlike wild-type cells
(J:205441)
• however, treatment with exogenous IL2 increased proliferation response
(J:205441)
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• after 96 hours in culture, only 68% of T cells are alive compared to 83% of controls
• more mutant T cells are apoptotic after radiation dosage than in controls
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• T cells have markedly impaired proliferation in response to T cell co-stimulation (anti-CD3 + anti-CD28)
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• alpha-galactosylceramide-induced cytotoxic activity of splenic and hepatic mononuclear cells was reduced compared to wild-type
• alpha-galactosylceramide-induced anti-metastatic effect was substantially reduced compared to wild-type, indicating that natural killer cells are not able to fight off cancer cells
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• alpha-galactosylceramide-induced serum IFN-gamma levels were reduced compared to wild-type
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• alpha-galactosylceramide-induced (an antigen that activates invariant natural killer T cells) serum IL-4 levels were reduced compared to wild-type
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• mice have reduced airway hyperresponsiveness after sensitization and challenge with OVA
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• T cells secrete less IL-2 when activated compared to controls
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• mice fail to develop EAE after immunization with MOG and even lack inflammatory infiltrates into the spinal cord
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• after 96 hours in culture, only 68% of T cells are alive compared to 83% of controls
• more mutant T cells are apoptotic after radiation dosage than in controls
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• T cells have markedly impaired proliferation in response to T cell co-stimulation (anti-CD3 + anti-CD28)
|
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• alpha-galactosylceramide-induced cytotoxic activity of splenic and hepatic mononuclear cells was reduced compared to wild-type
• alpha-galactosylceramide-induced anti-metastatic effect was substantially reduced compared to wild-type, indicating that natural killer cells are not able to fight off cancer cells
|
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• after 96 hours in culture, only 68% of T cells are alive compared to 83% of controls
• more mutant T cells are apoptotic after radiation dosage than in controls
|
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• T cells have markedly impaired proliferation in response to T cell co-stimulation (anti-CD3 + anti-CD28)
|
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• alpha-galactosylceramide-induced serum IFN-gamma levels were reduced compared to wild-type
|
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• alpha-galactosylceramide-induced (an antigen that activates invariant natural killer T cells) serum IL-4 levels were reduced compared to wild-type
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• T lymphocytes exhibit a reduced proliferative response to lectins
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• immunoglobulin class switching to neutralizing antibodies of the IgG class is reduced after infection with vesicular stomatitis virus
• however, induction of cytotoxic T cells still occurs and mutants show delayed-type hypersensitivity after infection with lymphocytic choriomeningitis virus
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• basal level of immunoglobulins is 20% that of wild-type
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• decrease in T helper cell activity
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• mutants exhibit reduced production of IL-2 in response to lectin stimulation
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• T lymphocytes exhibit a reduced proliferative response to lectins
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• immunoglobulin class switching to neutralizing antibodies of the IgG class is reduced after infection with vesicular stomatitis virus
• however, induction of cytotoxic T cells still occurs and mutants show delayed-type hypersensitivity after infection with lymphocytic choriomeningitis virus
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• basal level of immunoglobulins is 20% that of wild-type
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• decrease in T helper cell activity
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• T lymphocytes exhibit a reduced proliferative response to lectins
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• T cells stimulated in vitro proliferate much less than controls to anti-CD3
• T cells fail to proliferate when restimulated with OVA peptide
• T cells also produce less IL-2 during these in vitro stimulations
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• serum contains significantly less of the Th2-dependent anti-GAD IgG2a antibodies
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• Th1 responses are enhanced in these mice
• splenic T cells secrete high levels of IFN-gamma while expressing very little to no IL-4 upon stimulation
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• Th2 responses are dampened in these mice
• splenic T cells secrete high levels of IFN-gamma while expressing very little to no IL-4 upon stimulation
• serum contains significantly less of the Th2-dependent anti-GAD IgG2a antibodies
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• splenic T cells secrete high levels of IFN-gamma, sometimes as much as 4-fold compared to controls
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• T cells also produce less IL-2 during stimulation with anti-CD3 antibody or upon restimulation with OVA peptide
• T cells secrete the same amout of IL-2 as controls when stimulated with the diabetic autoantigen GAD
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• T cell secrete little to no IL-4 upon activation in vitro
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• 70-80% of female mice in the fourth backcross onto the NOD strain are hyperglycemic by 24 weeks of age compared to 30% for non-transgenic littermate controls
• nearly 90% of male mice in this backcross are hyperglycemic by 24 weeks of age compared to 10% of non-transgenic littermate controls
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• T cells also produce less IL-2 during these in vitro stimulations
• T cells stimulated in vitro proliferate much less than controls to anti-CD3
• T cells fail to proliferate when restimulated with OVA peptide
|
|
• serum contains significantly less of the Th2-dependent anti-GAD IgG2a antibodies
|
|
• Th1 responses are enhanced in these mice
• splenic T cells secrete high levels of IFN-gamma while expressing very little to no IL-4 upon stimulation
|
|
• Th2 responses are dampened in these mice
• splenic T cells secrete high levels of IFN-gamma while expressing very little to no IL-4 upon stimulation
• serum contains significantly less of the Th2-dependent anti-GAD IgG2a antibodies
|
|
• T cells stimulated in vitro proliferate much less than controls to anti-CD3
• T cells fail to proliferate when restimulated with OVA peptide
• T cells also produce less IL-2 during these in vitro stimulations
|
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• expansion of transferred CD25-depleted T cells from Tg(TcraBDC2.5)1Doi Tg(TcrbBDC2.5)2Doi is dramatically accelerated compared to NOD controls; there are 5-fold more autoreactive transferred T cells in pancreatic lymph nodes compared to NOD mice
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• only 1.5% of CD4 T cells in homozygotes express CD25 compared to 6.5% in wild-type
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• mice show higher incidence of diabetes compared to Cd40lg, Cd28 double null mice
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• CD28-deficient NOD mice injected with CD4+CD25+ NOD T cells showed significant delay in the development of diabetes with no disease apparent through 15 weeks of age, whereas transfer of CD4+CD25+ T cells resulted in diabetes development by 11 weeks of age
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• expansion of transferred CD25-depleted T cells from Tg(TcraBDC2.5)1Doi Tg(TcrbBDC2.5)2Doi is dramatically accelerated compared to NOD controls; there are 5-fold more autoreactive transferred T cells in pancreatic lymph nodes compared to NOD mice
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• only 1.5% of CD4 T cells in homozygotes express CD25 compared to 6.5% in wild-type
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• expansion of transferred CD25-depleted T cells from Tg(TcraBDC2.5)1Doi Tg(TcrbBDC2.5)2Doi is dramatically accelerated compared to NOD controls; there are 5-fold more autoreactive transferred T cells in pancreatic lymph nodes compared to NOD mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• a marked defect in proliferative response to anti-CD3 alone and to the combination of anti-CD3 + anti-CD28
(J:124570)
• T cells have impaired proliferation in response to T cell co-stimulation (anti-CD3 + anti-CD28) that can be partially rescued by high level of anti-CD28 antibody
(J:149888)
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• a mixed lymphocyte culture with alloantigen failed to proliferate
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• mutant mice sensitized and challenged with OVA fails to develop germinal centers in the spleen
• mutant animals show a normal inflammatory response to OVA stimulation
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• mutant mice sensitized and challenged with OVA shows a marked decrease in OVA-specific antibody
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• a substantial reduction in the amount of several cytokines in the culture supernatants of stimulated T cells
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• no detectable IL-2 present in the culture supernatants of stimulated T cells
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• a marked defect in proliferative response to anti-CD3 alone and to the combination of anti-CD3 + anti-CD28
(J:124570)
• T cells have impaired proliferation in response to T cell co-stimulation (anti-CD3 + anti-CD28) that can be partially rescued by high level of anti-CD28 antibody
(J:149888)
|
|
• a mixed lymphocyte culture with alloantigen failed to proliferate
|
|
• mutant mice sensitized and challenged with OVA fails to develop germinal centers in the spleen
• mutant animals show a normal inflammatory response to OVA stimulation
|
|
• mutant mice sensitized and challenged with OVA shows a marked decrease in OVA-specific antibody
|
|
• a marked defect in proliferative response to anti-CD3 alone and to the combination of anti-CD3 + anti-CD28
(J:124570)
• T cells have impaired proliferation in response to T cell co-stimulation (anti-CD3 + anti-CD28) that can be partially rescued by high level of anti-CD28 antibody
(J:149888)
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• CD4 T cells proliferate in vitro at normal levels when stimulated with anti-CD3 antibody compared
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• increased number of CD44highCD62low T cells in the spleen and lymph nodes
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• increased number of CD69+ T cells are found in the spleen and lymph nodes
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• CD4 T cells secrete IL-2 upon stimulation with anti -CD3 or -CD3/-CD28 antibodies
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• CD4 T cells proliferate in vitro at normal levels when stimulated with anti-CD3 antibody compared
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• increased number of CD44highCD62low T cells in the spleen and lymph nodes
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• increased number of CD69+ T cells are found in the spleen and lymph nodes
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• CD4 T cells proliferate in vitro at normal levels when stimulated with anti-CD3 antibody compared
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• Nippostrongylus brasiliensis fecundity was not depressed in experimental infections
• spontaneous Desmodex infections develop in 4-8 months
• severe dermatitis develops as a result of infection
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice show partial rescue of Vbeta11+CD4+ thymocytes from negative selection
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• mice show partial rescue of Vbeta11+CD4+ thymocytes from negative selection
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice show partial rescue of Vbeta11+CD4+ thymocytes from negative selection
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• CD4+ thymocytes are increased to a greater extent than in CD5 knockouts
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• Cd8+ thymocytes are increased
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• mice show partial rescue of Vbeta11+CD4+ thymocytes from negative selection
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• CD4+ thymocytes are increased to a greater extent than in CD5 knockouts
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• Cd8+ thymocytes are increased
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice show partial rescue of Vbeta11+CD4+ thymocytes from negative selection
|
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• mice show partial rescue of Vbeta11+CD4+ thymocytes from negative selection
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mutants exhibit weaker cytotoxic T cell responses to influenza virus, but have unimpaired responses to lymphocytic chriomeningitis virus
|
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• mutants exhibit a delay in skin allograft rejection of up to 14 days
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• mutants exhibit weaker cytotoxic T cell responses to influenza virus, but have unimpaired responses to lymphocytic chriomeningitis virus
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• later with lesser eosinophil infiltration than in Ndfip1Gt(RRD002)Byg homozygotes
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• in the small bowel, but not esophagus
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• following T cell activation
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• following T cell activation
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• epithelial hypertrophy in the esophagus
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• later with lesser eosinophil infiltration than in Ndfip1Gt(RRD002)Byg homozygotes
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• in the small bowel, but not esophagus
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mutants show a longer skin graft survival of about 6 days than wild-type mice or single homozygotes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 2 of 22 double mutants develop T cell lymphoma
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• tumor incidence (about 10%) is reduced compared to Rc3h1 heterozygotes (more than 50%)
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• 2 of 22 double mutants develop T cell lymphoma
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• CD8 T cells require 10- to 100-fold more antigen (gp33 peptide) to induce the same amount of proliferation as cells from Tg(TcrLCMV)327Sdz mice
• however, addition of IL2 restores CD8 T cell proliferation in response to gp33 peptide
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• in mice treated gp33 peptide
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• after 3 days, cytotoxic T lymphocyte (CTL) activation in mice treated with gp33 peptide is decreased compared to in Tg(TcrLCMV)327Sdz mice
• splenocytes exposed to gp33 exhibit impaired CTL activation compared with similarly treated cells from Tg(TcrLCMV)327Sdz mice
• however, CTL activation in mice treated with gp33 peptide is normal at day 1 and treatment with IL2 restores CTL in splenocytes
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• cytotoxic T lymphocyte anergy in mice treated with gp33 peptide is induced unlike in similarly treated Tg(TcrLCMV)327Sdz mice
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• CD8 T cells require 10- to 100-fold more antigen (gp33 peptide) to induce the same amount of proliferation as cells from Tg(TcrLCMV)327Sdz mice
• however, addition of IL2 restores CD8 T cell proliferation in response to gp33 peptide
|
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• in mice treated gp33 peptide
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• after 3 days, cytotoxic T lymphocyte (CTL) activation in mice treated with gp33 peptide is decreased compared to in Tg(TcrLCMV)327Sdz mice
• splenocytes exposed to gp33 exhibit impaired CTL activation compared with similarly treated cells from Tg(TcrLCMV)327Sdz mice
• however, CTL activation in mice treated with gp33 peptide is normal at day 1 and treatment with IL2 restores CTL in splenocytes
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• CD8 T cells require 10- to 100-fold more antigen (gp33 peptide) to induce the same amount of proliferation as cells from Tg(TcrLCMV)327Sdz mice
• however, addition of IL2 restores CD8 T cell proliferation in response to gp33 peptide
|
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• in mice treated gp33 peptide
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• compared to wild-type Cd28 transgenic mice Cd28-deficient mice show no lymphocyte expansion or increase in CD8+ T cell population
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• compared to wild-type Cd28 transgenic mice Cd28-deficient mice show no lymphocyte expansion or increase in CD8+ T cell population
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
 |
• mice display a dramatic reduction in numbers of Tregs compared to NOD controls and Cd40lg-deficiet NOD mice
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• mice show increased incidence of diabetes (blood glucose level >300 mg/dl) compared to Cd40lg-deficient NOD mice
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• mice display a dramatic reduction in numbers of Tregs compared to NOD controls and Cd40lg-deficiet NOD mice
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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 04/16/2024 MGI 6.23 |
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