Phenotypes associated with this allele
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Eomestm1Srnr mutation
(1 available);
any
Eomes mutation
(41 available)
Tg(Cd4-cre)1Cwi mutation
(10 available)
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immune system
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N |
• unlike mice with T-cell specific conditional deletion of Eomes that also lack expression of Tbx21, clearance of lymphocyte choriomeningitis virus is similar to wild-type controls
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• deficiency in memory-phenotype CD8+ T cells
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hematopoietic system
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• deficiency in memory-phenotype CD8+ T cells
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Eomestm1Srnr mutation
(1 available);
any
Eomes mutation
(41 available)
Tbx21tm1Srnr mutation
(0 available);
any
Tbx21 mutation
(36 available)
Tg(Cd4-cre)1Cwi mutation
(10 available)
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immune system
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• impaired cytotoxic CD8+ T cell differentiation following viral infection
• following viral infection, differentiation is skewed exclusively toward the Type 17 fate
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• defect in accumulation of CD8+ T cells following viral infection
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• deficiency in memory-phenotype CD8+ T cells
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• CD8+ T cells have a severe defect in cytotoxic gene expression in response to viral peptide stimulation even when cellularity is normalized
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• increase in IL17 expression in CD8+ T cells in response to stimulation with viral derived peptides
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• persistent high titers of lymphocyte choriomeningitis virus
• progressive weight loss, not seen in controls, begins about 1 week after infection and is accompanied by extensive organ pathology and excessive neutrophil response
• depletion of CD8+ T cells prevents viral induced wasting, neutrophilia, and organ pathology
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homeostasis/metabolism
hematopoietic system
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• impaired cytotoxic CD8+ T cell differentiation following viral infection
• following viral infection, differentiation is skewed exclusively toward the Type 17 fate
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• defect in accumulation of CD8+ T cells following viral infection
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• deficiency in memory-phenotype CD8+ T cells
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• CD8+ T cells have a severe defect in cytotoxic gene expression in response to viral peptide stimulation even when cellularity is normalized
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Analysis Tools