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促凋亡bcl-2家族成员bim介导的体内活化T细胞死亡。

Activated T cell death in vivo mediated by proapoptotic bcl-2 family member bim.

作者信息

Hildeman David A, Zhu Yanan, Mitchell Thomas C, Bouillet Philippe, Strasser Andreas, Kappler John, Marrack Philippa

机构信息

Howard Hughes Medical Institute and Department of Medicine, National Jewish Medical and Research Center, Denver, CO 80206, USA.

出版信息

Immunity. 2002 Jun;16(6):759-67. doi: 10.1016/s1074-7613(02)00322-9.

Abstract

At the end of the T cell response, the majority of the activated T cells die. We activated Vbeta8(+) T cells with staphylococcal enterotoxin B (SEB) in vivo and monitored the expansion and deletion of Vbeta8(+) T cells. We found that, in response to SEB, activated T cells died in vivo in the absence of Fas or TNF-R signaling but not when they overexpressed human Bcl-2. We also found that Vbeta8(+) T cells from Bim-deficient mice are resistant to SEB-induced deletion. While Bim levels did not change, endogenous Bcl-2 levels within Vbeta8(+) T cells decrease following SEB injection. Thus, the death of superantigen-stimulated T cells in vivo is mediated by Bim and may be modulated by a decrease in Bcl-2.

摘要

在T细胞应答结束时,大多数活化的T细胞会死亡。我们在体内用葡萄球菌肠毒素B(SEB)激活Vβ8(+) T细胞,并监测Vβ8(+) T细胞的扩增和缺失情况。我们发现,对SEB的应答中,活化的T细胞在缺乏Fas或TNF-R信号传导时会在体内死亡,但当它们过表达人Bcl-2时则不会。我们还发现,来自Bim缺陷小鼠的Vβ8(+) T细胞对SEB诱导的缺失具有抗性。虽然Bim水平没有变化,但SEB注射后Vβ8(+) T细胞内源性Bcl-2水平会降低。因此,体内超抗原刺激的T细胞死亡是由Bim介导的,并且可能受到Bcl-2减少的调节。

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