Shutdown of an acute T cell immune response to viral infection is mediated by the proapoptotic Bcl-2 homology 3-only protein Bim
Shutdown of an acute T cell immune response to viral infection is mediated by the proapoptotic Bcl-2 homology 3-only protein Bim
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DOI：
10.1073/pnas.2336198100
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发表时间：
2003-11-25
影响因子：
11.1
通讯作者：
Strasser, A
中科院分区：
文献类型：
--
作者：
Pellegrini, M;Belz, G;Strasser, A
我们使用突变型Fas缺陷（lpr）或Bim缺陷小鼠来研究死亡受体和Bcl-2调节的凋亡途径在终止单纯疱疹病毒感染的生理性T细胞应答中的作用。在WT和lpr小鼠中，病毒清除后，CD 8（+）抗原特异性T细胞被删除。相反，尽管病毒被清除，但Bim缺陷小鼠的免疫应答并未终止，CD 8（+）抗原特异性T细胞在脾脏中积累。因此，Bim被用于病毒清除，但当免疫应答终止时，对于活化的T细胞的死亡是必需的。这些发现对感染和免疫的免疫反应的治疗操作具有影响。
We used mutant Fas-deficient (lpr) or Bim-deficient mice to investigate the role of the death receptor and Bcl-2-regulated apoptotic pathways in terminating a physiological T cell response to herpes simplex virus infection. In WT and lpr mice CD8(+) antigen-specific T cells were deleted after viral clearance. In contrast, the immune response was not terminated in Bim-deficient mice despite viral clearance, and CD8(+) antigen-specific T cells accumulated in the spleen. Thus, Bim is dispensable for viral clearance but is necessary for the death of activated T cells when immune responses are terminated. These findings have implications for the therapeutic manipulation of immune responses to infections and immunization.