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• W1490805439 endingPage "5282" @default.
• W1490805439 startingPage "5275" @default.
• W1490805439 abstract "Abstract The maintenance of T cell tolerance in the periphery proceeds through several mechanisms, including anergy, immuno-regulation, and deletion via apoptosis. We examined the mechanism underlying the induction of CD8 T cell peripheral tolerance to a self-Ag expressed on pancreatic islet β-cells. Following adoptive transfer, Ag-specific clone 4 T cells underwent deletion independently of extrinsic death receptors, including Fas, TNFR1, or TNFR2. Additional experiments revealed that the induction of clone 4 T cell apoptosis during peripheral tolerance occurred via an intrinsic death pathway that could be inhibited by overexpression of Bcl-2 or targeted deletion of the proapoptotic molecule, Bim, thereby resulting in accumulation of activated clone 4 T cells. Over-expression of Bcl-2 in clone 4 T cells promoted the development of effector function and insulitis whereas Bim−/− clone 4 cells were not autoaggressive. Examination of the upstream molecular mechanisms contributing to clone 4 T cell apoptosis revealed that it proceeded in a p53, E2F1, and E2F2-independent manner. Taken together, these data reveal that initiation of clone 4 T cell apoptosis during the induction of peripheral tolerance to a cross-presented self-Ag occurs through a Bcl-2-sensitive and at least partially Bim-dependent mechanism." @default.
• W1490805439 created "2016-06-24" @default.
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• W1490805439 date "2008-04-15" @default.
• W1490805439 modified "2023-10-17" @default.
• W1490805439 title "The Apoptotic Pathway Contributing to the Deletion of Naive CD8 T Cells during the Induction of Peripheral Tolerance to a Cross-Presented Self-Antigen" @default.
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• W1490805439 doi "https://doi.org/10.4049/jimmunol.180.8.5275" @default.
• W1490805439 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7703405" @default.
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• W1490805439 hasPublicationYear "2008" @default.
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