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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >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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Shutdown of an acute T cell immune response to viral infection is mediated by the proapoptotic Bcl-2 homology 3-only protein Bim

机译:凋亡的Bcl-2同源性3-only蛋白Bim介导对病毒感染的急性T细胞免疫反应的关闭

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摘要

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.
机译: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对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,CD8 +抗原特异性T细胞被删除。相反,尽管有病毒清除,但在Bim缺陷小鼠中免疫应答并未终止,并且CD8〜+抗原特异性T细胞在脾脏中积累。因此,Bim对于病毒清除是必不可少的,但在免疫反应终止时对于活化的T细胞的死亡是必不可少的。这些发现对对感染和免疫的免疫反应的治疗性操作具有影响。

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