期刊
IMMUNOLOGIC RESEARCH
卷 41, 期 2, 页码 137-153出版社
HUMANA PRESS INC
DOI: 10.1007/s12026-008-8017-1
关键词
T cells; MHC; sensitization; desensitization; cell cycle; negative regulation; tolerance
类别
资金
- NCI NIH HHS [P30 CA046934, P30 CA046934-200007, P30 CA 46934, P30 CA046934-190007] Funding Source: Medline
- NIDDK NIH HHS [R21 DK 63410, R21 DK063410-02, R01 DK058722-01, R01 DK058722-03, R01 DK058722, R01 DK 58722, R21 DK063410-01, R01 DK058722-04, R01 DK058722-02, R21 DK063410] Funding Source: Medline
It is now apparent that naive peripheral T cells are a dynamic population where active processes prevent inappropriate activation while supporting survival. The process of thymic education makes naive peripheral T cells dependent on interactions with self-MHC for survival. However, as these signals can potentially result in inappropriate activation, various non-redundant, intrinsic negative regulatory molecules including Tob, Nfatc2, and Smad3 actively enforce T cell quiescence. Interactions among these pathways are only now coming to light and may include positive or negative crosstalk. In the case of positive crosstalk, self-MHC initiated signals and intrinsic negative regulatory factors may cooperate to dampen T cell activation and sustain peripheral tolerance in a binary fashion (on-off). In the case of negative crosstalk, self-MHC signals may promote survival through partial activation while intrinsic negative regulatory factors act as rheostats to restrain cell cycle entry and prevent T cells from crossing a threshold that would break tolerance.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据