Reactive oxygen species regulate activation-induced T cell apoptosis

被引:422
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
相关论文
共 56 条
  • [1] [Anonymous], 1985, Free Radicals in Biology and Medicine (Eds)
  • [2] Fas-induced activation of the cell death-related protease CPP32 is inhibited by Bcl-2 and by ICE family protease inhibitors
    Armstrong, RC
    Aja, T
    Xiang, JL
    Gaur, S
    Krebs, JF
    Hoang, K
    Bai, X
    Korsmeyer, J
    Karanewsky, DS
    Fritz, LC
    Tomaselli, KJ
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (28) : 16850 - 16855
  • [3] CELL-AUTONOMOUS FAS (CD95) FAS-LIGAND INTERACTION MEDIATES ACTIVATION-INDUCED APOPTOSIS IN T-CELL HYBRIDOMAS
    BRUNNER, T
    MOGIL, RJ
    LAFACE, D
    YOO, NJ
    MAHBOUBI, A
    ECHEVERRI, F
    MARTIN, SJ
    FORCE, WR
    LYNCH, DH
    WARE, CF
    GREEN, DR
    [J]. NATURE, 1995, 373 (6513) : 441 - 444
  • [4] REDOX REGULATION OF PROGRAMMED CELL-DEATH IN LYMPHOCYTES - INVITED COMMENTARY
    BUTTKE, TM
    SANDSTROM, PA
    [J]. FREE RADICAL RESEARCH, 1995, 22 (05) : 389 - 397
  • [5] Oxidant, mitochondria and calcium: An overview
    Chakraborti, T
    Mondal, M
    Roychoudhury, S
    Chakraborti, S
    [J]. CELLULAR SIGNALLING, 1999, 11 (02) : 77 - 85
  • [6] Caspases: the executioners of apoptosis
    Cohen, GM
    [J]. BIOCHEMICAL JOURNAL, 1997, 326 : 1 - 16
  • [7] Day BJ, 1995, J PHARMACOL EXP THER, V275, P1227
  • [8] Manganic porphyrins possess catalase activity and protect endothelial cells against hydrogen peroxide-mediated injury
    Day, BJ
    Fridovich, I
    Crapo, JD
    [J]. ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 1997, 347 (02) : 256 - 262
  • [9] Déas O, 1998, J IMMUNOL, V161, P3375
  • [10] AUTOCRINE T-CELL SUICIDE MEDIATED BY APO-1/(FAS/CD95)
    DHEIN, J
    WALCZAK, H
    BAUMLER, C
    DEBATIN, KM
    KRAMMER, PH
    [J]. NATURE, 1995, 373 (6513) : 438 - 441