Reactive oxygen species regulate activation-induced T cell apoptosis

被引:423
作者
Hildeman, DA
Mitchell, T
Teague, TK
Henson, P
Day, BJ
Kappler, J
Marrack, PC
机构
[1] Univ Colorado, Hlth Sci Ctr, Natl Jewish Med & Res Ctr, Howard Hughes Med Inst, Denver, CO 80206 USA
[2] Univ Colorado, Hlth Sci Ctr, Natl Jewish Med & Res Ctr, Dept Med, Denver, CO 80206 USA
[3] Univ Colorado, Hlth Sci Ctr, Natl Jewish Med & Res Ctr, Dept Pediat, Denver, CO 80206 USA
[4] Univ Colorado, Hlth Sci Ctr, Dept Pharmaceut Sci, Denver, CO 80206 USA
[5] Univ Colorado, Hlth Sci Ctr, Dept Pharmacol, Denver, CO 80206 USA
[6] Univ Colorado, Hlth Sci Ctr, Dept Biochem Biophys & Genet, Denver, CO 80206 USA
[7] Univ Colorado, Hlth Sci Ctr, Dept Immunol & Med, Denver, CO 80206 USA
关键词
D O I
10.1016/S1074-7613(00)80072-2
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Reactive oxygen species (ROS) mediate apoptosis in a number of cell types. We studied the role that ROS play in activated T cell apoptosis by activating T cells in vivo and then culturing them for a short time. Activated T cells died independently of Fas and TNF alpha. Their death was characterized by rapid loss of mitochondrial transmembrane potential (Delta psi(m)), caspase-dependent DNA fragmentation, and superoxide generation. A superoxide dismutase mimetic, Mn (III) tetrakis (5, 10, 15, 20-benzoic acid) porphyrin (MnTBAP), protected T cells from superoxide generation, caspase-dependent DNA loss, loss of Delta psi(m), and cell death. These results indicate that ROS can regulate signals involved in caspase activation and apoptosis and may contribute to peripheral T cell deletion.
引用
收藏
页码:735 / 744
页数:10
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