期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 196, 期 7, 页码 947-955出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20020827
关键词
CD8-positive T lymphocytes; antigen presentation; T cell tolerance; Bcl-2; apoptosis
资金
- NIAID NIH HHS [AI43347] Funding Source: Medline
By transgenic expression of ovalbumin (OVA) as a model self antigen in the beta cells of the pancreas, we have shown that self tolerance can be maintained by the cross-presentation of this antigen on dendritic cells in the draining lymph nodes. Such cross-presentation causes initial activation of OVA-specific CD8 T cells, which proliferate but are ultimately deleted; a process referred to as cross-tolerance. Here, we investigated the molecular basis of cross-tolerance. Deletion of CD8 T cells was prevented by overexpression of Bcl-2, indicating that cross-tolerance was mediated by a Bcl-2 inhibitable pathway. Recently, Bim, a pro-apoptotic Bcl-2 family member whose function can be inhibited by Bcl-2, was found to play a critical role in the deletion of autoreactive thymocytes, leading us to examine its role in cross-tolerance. Bim-deficient T cells were not deleted in response to cross-presented self-antigen, strongly implicating Bim as the pro-apoptotic mediator of cross-tolerance.
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