A regulatory role for TRAF1 in antigen-induced apoptosis of T cells

被引:116
作者
Speiser, DE
Lee, SY
Wong, B
Arron, J
Santana, A
Kong, YY
Ohashi, PS
Choi, Y
机构
[1] ROCKEFELLER UNIV, HOWARD HUGHES MED INST, NEW YORK, NY 10021 USA
[2] ONTARIO CANC INST, DEPT MED BIOPHYS, TORONTO, ON M5G 2M9, CANADA
[3] ONTARIO CANC INST, DEPT IMMUNOL, TORONTO, ON M5G 2M9, CANADA
关键词
D O I
10.1084/jem.185.10.1777
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Tumor necrosis factor receptor (TNFR)-associated factor 2 (TRAF2) and TRAF1 were found as components of the TNFR2 signaling complex, which exerts multiple biological effects on cells such as cell proliferation, cytokine production, and cell death. In the TNFR2-mediated. signaling pathways, TRAF2 works as a mediator for activation signals such as NF-KB, but the role of TRAF1 has not been previously determined. Here we show in transgenic mice that TRAF1 overexpression inhibits antigen-induced apoptosis of CD8(+) T lymphocytes. Our results demonstrate a biological role for TRAF1 as a regulator of apoptotic signals and also support the hypothesis that the combination of TRAF proteins in a given cell type determines distinct biological effects triggered by members of the TNF receptor superfamily.
引用
收藏
页码:1777 / 1783
页数:7
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