Activated T cell death in vivo mediated by proapoptotic Bcl-2 family member Bim

被引:467
作者
Hildeman, DA
Zhu, YN
Mitchell, TC
Bouillet, P
Strasser, A
Kappler, J
Marrack, P
机构
[1] Univ Colorado, Hlth Sci Ctr, Howard Hughes Med Inst, Denver, CO 80206 USA
[2] Univ Colorado, Hlth Sci Ctr, Dept Med, Natl Jewish Med & Res Ctr, Denver, CO 80206 USA
[3] Univ Colorado, Hlth Sci Ctr, Dept Biochem & Mol Genet, Denver, CO 80206 USA
[4] Univ Louisville, Hlth Sci Ctr, Sch Med, Inst Cellular Therapeut, Louisville, KY 40202 USA
[5] Walter & Eliza Hall Inst Med Res, Melbourne, Vic 3050, Australia
[6] Univ Colorado, Hlth Sci Ctr, Dept Integrat Immunol, Denver, CO 80206 USA
[7] Univ Colorado, Hlth Sci Ctr, Dept Pharmacol, Denver, CO 80206 USA
关键词
D O I
10.1016/S1074-7613(02)00322-9
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:759 / 767
页数:9
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