cFLIP regulation of lymphocyte activation and development

被引:231
作者
Budd, RC [1 ]
Yeh, WC
Tschopp, J
机构
[1] Univ Vermont, Dept Med, Program Immunol, Burlington, VT 05405 USA
[2] Univ Toronto, Cambell Family Inst Brest Canc Res, Univ Hlth Network, Dept Med Biophys, Toronto, ON M5G 2C1, Canada
[3] Univ Lausanne, Dept Biochem, BIL Biomed Res Ctr, CH-1066 Epalinges, Switzerland
基金
美国国家卫生研究院; 加拿大健康研究院;
关键词
D O I
10.1038/nri1787
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Cellular caspase-8 (FLICE)-like inhibitory protein (cFLIP) was originally identified as an inhibitor of death-receptor signalling through competition with caspase-8 for recruitment to FAS-associated via death domain ( FADD). More recently, it has been determined that both cFLIP and caspase-8 are required for the survival and proliferation of T cells following T-cell-receptor stimulation. This paradoxical finding launched new investigations of how these molecules might connect with signalling pathways that link to cell survival and growth following antigen-receptor activation. As discussed in this Review, insight gained from these studies indicates that cFLIP and caspase-8 form a heterodimer that ultimately links T-cell receptor signalling to activation of nuclear factor-kappa B through a complex that includes B-cell lymphoma 10 (BCL-10), mucosa-associated-lymphoid-tissue lymphoma-translocation gene 1 (MALT1) and receptor- interacting protein 1 (RIP1).
引用
收藏
页码:196 / 204
页数:9
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