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• W2163469328 startingPage "4994" @default.
• W2163469328 abstract "Abstract TCR and cytokine receptor signaling play key roles in the complex homeostatic mechanisms that maintain a relative stable number of T cells throughout life. Despite the homeostatic mechanisms, a slow decline in naive T cells is typically observed with age. The CD3γ di-leucine-based motif controls TCR down-regulation and plays a central role in fine-tuning TCR expression and signaling in T cells. In this study, we show that the age-associated decline of naive T cells is strongly accelerated in CD3γLLAA knock-in mice homozygous for a double leucine to alanine mutation in the CD3γ di-leucine-based motif, whereas the number of memory T cells is unaffected by the mutation. This results in premature T cell population senescence with a severe dominance of memory T cells and very few naive T cells in middle-aged to old CD3γ mutant mice. The reduced number of naive T cells in CD3γ mutant mice was caused by the combination of reduced thymic output, decreased T cell apoptosis, and increased transition of naive T cells to memory T cells. Experiments with bone marrow chimeric mice confirmed that the CD3γLLAA mutation exerted a T cell intrinsic effect on T cell homeostasis that resulted in an increased transition of CD3γLLAA naive T cells to memory T cells and a survival advantage of CD3γLLAA T cells compared with wild-type T cells. The experimental observations were further supported by mathematical modeling of T cell homeostasis. Our study thus identifies an important role of CD3γ-mediated TCR down-regulation in T cell homeostasis." @default.
• W2163469328 created "2016-06-24" @default.
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• W2163469328 date "2009-10-15" @default.
• W2163469328 modified "2023-10-14" @default.
• W2163469328 title "TCR Down-Regulation Controls T Cell Homeostasis" @default.
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• W2163469328 doi "https://doi.org/10.4049/jimmunol.0901539" @default.
• W2163469328 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19801521" @default.
• W2163469328 hasPublicationYear "2009" @default.
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