Molecular mechanisms of activated T cell death in vivo

被引:197
作者
Hildeman, DA
Zhu, YN
Mitchell, TC
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 Colorado, Hlth Sci Ctr, Dept Integrated Immunol, Denver, CO 80206 USA
[5] Univ Colorado, Hlth Sci Ctr, Dept Pharmacol, Denver, CO 80206 USA
[6] Univ Louisville, Sch Med, Inst Cellular Therapeut, Louisville, KY 40202 USA
关键词
D O I
10.1016/S0952-7915(02)00335-7
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The culmination of the immune response involves the death of the majority of the activated antigen-specific T lymphocytes. The death of these cells is important to prevent autoimmunity, to decrease the metabolic cost to the organism and to ensure T cell homeostasis. This review will focus on the mechanisms that, in animals, control the death of these activated cells. At least two separate types of cell death can occur (activation-induced cell death and activated T cell autonomous death) via death receptors such as Fas or the Bcl-2 related protein Bim, respectively. Finally, adjuvants that enable T cell survival may operate via NF-kappaB and Bcl-3 rather than cytokines.
引用
收藏
页码:354 / 359
页数:6
相关论文
共 34 条
[1]  
Algeciras-Schimnich A, 1999, J IMMUNOL, V162, P5205
[2]   CELL-GROWTH CYCLE BLOCK OF T-CELL HYBRIDOMAS UPON ACTIVATION WITH ANTIGEN [J].
ASHWELL, JD ;
CUNNINGHAM, RE ;
NOGUCHI, PD ;
HERNANDEZ, D .
JOURNAL OF EXPERIMENTAL MEDICINE, 1987, 165 (01) :173-194
[3]   Proapoptotic Bcl-2 relative bim required for certain apoptotic responses, leukocyte homeostasis, and to preclude autoimmunity [J].
Bouillet, P ;
Metcalf, D ;
Huang, DCS ;
Tarlinton, DM ;
Kay, TWH ;
Köntgen, F ;
Adams, JM ;
Strasser, A .
SCIENCE, 1999, 286 (5445) :1735-1738
[4]   BH3-only Bcl-2 family member Bim is required for apoptosis of autoreactive thymocytes [J].
Bouillet, P ;
Purton, JF ;
Godfrey, DI ;
Zhang, LC ;
Coultas, L ;
Puthalakath, H ;
Pellegrini, M ;
Cory, S ;
Adams, JM ;
Strasser, A .
NATURE, 2002, 415 (6874) :922-926
[5]   4-1BB ligand induces cell division, sustains survival, and enhances effector function of CD4 and CD8 T cells with similar efficacy [J].
Cannons, JL ;
Lau, P ;
Ghumman, B ;
DeBenedette, MA ;
Yagita, H ;
Okumura, K ;
Watts, TH .
JOURNAL OF IMMUNOLOGY, 2001, 167 (03) :1313-1324
[6]   Requirement for transforming growth factor β1 in controlling T cell apoptosis [J].
Chen, WJ ;
Jin, WW ;
Tian, HS ;
Sicurello, P ;
Frank, M ;
Orenstein, JM ;
Wahl, SM .
JOURNAL OF EXPERIMENTAL MEDICINE, 2001, 194 (04) :439-453
[7]   BCL-2, BCL-XL sequester BH3 domain-only molecules preventing BAX- and BAK-mediated mitochondrial apoptosis [J].
Cheng, EHYA ;
Wei, MC ;
Weiler, S ;
Flavell, RA ;
Mak, TW ;
Lindsten, T ;
Korsmeyer, SJ .
MOLECULAR CELL, 2001, 8 (03) :705-711
[8]  
DUKE RC, 1986, LYMPHOKINE RES, V5, P289
[9]   A SINGLE INJECTION OF STAPHYLOCOCCUS-AUREUS ENTEROTOXIN-B REDUCES AUTOIMMUNITY IN MRL/LPR MICE [J].
GONZALO, JA ;
TARAZONA, R ;
SCHUURMAN, HJ ;
UYTDEHAAG, F ;
WICK, G ;
MARTINEZ, C ;
KROEMER, G .
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY, 1994, 71 (02) :176-182
[10]   Molecular steps of death receptor and mitochondrial pathways of apoptosis [J].
Gupta, S .
LIFE SCIENCES, 2001, 69 (25-26) :2957-2964