FAS LIGAND MEDIATES ACTIVATION-INDUCED CELL-DEATH IN HUMAN T-LYMPHOCYTES

被引:874
作者
ALDERSON, MR
TOUGH, TW
DAVISSMITH, T
BRADDY, S
FALK, B
SCHOOLEY, KA
GOODWIN, RG
SMITH, CA
RAMSDELL, F
LYNCH, DH
机构
[1] Immunex Research and Developmental Corporation, Seattle, WA
关键词
D O I
10.1084/jem.181.1.71
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 [免疫学];
摘要
A significant proportion of previously activated human T cells undergo apoptosis when triggered through the CD3/T cell receptor complex, a process termed activation-induced cell death (AICD). Ligation of pas on activated T cells by either Fas antibodies or recombinant human Fas-ligand (Fas-L) also results in cytolysis. We demonstrate that these two pathways of apoptosis are causally related. Stimulation of previously activated T cells resulted in the expression of Fas-L mRNA and lysis of Fas-positive target cells. Fas-L antagonists inhibited AICD of T cell clones and staphylococcus enterotoxin B (SEB)-specific T cell lines. The data indicate AICD in previously stimulated T cells is mediated by Fas/Fas-L interactions.
引用
收藏
页码:71 / 77
页数:7
相关论文
共 43 条
[1]
ABERRANT TRANSCRIPTION CAUSED BY THE INSERTION OF AN EARLY TRANSPOSABLE ELEMENT IN AN INTRON OF THE FAS ANTIGEN GENE OF LPR MICE [J].
ADACHI, M ;
WATANABEFUKUNAGA, R ;
NAGATA, S .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (05) :1756-1760
[2]
FAS TRANSDUCES ACTIVATION SIGNALS IN NORMAL HUMAN T-LYMPHOCYTES [J].
ALDERSON, MR ;
ARMITAGE, RJ ;
MARASKOVSKY, E ;
TOUGH, TW ;
ROUX, E ;
SCHOOLEY, K ;
RAMSDELL, F ;
LYNCH, DH .
JOURNAL OF EXPERIMENTAL MEDICINE, 1993, 178 (06) :2231-2235
[3]
BOSSU P, 1993, J IMMUNOL, V151, P7233
[4]
CARLSSON R, 1988, J IMMUNOL, V140, P2484
[5]
LPR AND GLD - SINGLE GENE MODELS OF SYSTEMIC AUTOIMMUNITY AND LYMPHOPROLIFERATIVE DISEASE [J].
COHEN, PL ;
EISENBERG, RA .
ANNUAL REVIEW OF IMMUNOLOGY, 1991, 9 :243-269
[6]
THYMIC AND PERIPHERAL APOPTOSIS OF ANTIGEN-SPECIFIC T-CELLS MIGHT COOPERATE IN ESTABLISHING SELF TOLERANCE [J].
DADAMIO, L ;
AWAD, KM ;
REINHERZ, EL .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1993, 23 (03) :747-753
[7]
ACTIVATION WITH SUPERANTIGENS INDUCES PROGRAMMED DEATH IN ANTIGEN-PRIMED CD4+ CLASS-II+ MAJOR HISTOCOMPATIBILITY COMPLEX T-LYMPHOCYTES VIA A CD11A/CD18-DEPENDENT MECHANISM [J].
DAMLE, NK ;
LEYTZE, G ;
KLUSSMAN, K ;
LEDBETTER, JA .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1993, 23 (07) :1513-1522
[8]
ANALYSIS AND DISCRIMINATION OF NECROSIS AND APOPTOSIS (PROGRAMMED CELL-DEATH) BY MULTIPARAMETER FLOW-CYTOMETRY [J].
DIVE, C ;
GREGORY, CD ;
PHIPPS, DJ ;
EVANS, DL ;
MILNER, AE ;
WYLLIE, AH .
BIOCHIMICA ET BIOPHYSICA ACTA, 1992, 1133 (03) :275-285
[9]
T-CELL STIMULATION BY STAPHYLOCOCCAL ENTEROTOXINS - CLONALLY VARIABLE RESPONSE AND REQUIREMENT FOR MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-II MOLECULES ON ACCESSORY OR TARGET-CELLS [J].
FLEISCHER, B ;
SCHREZENMEIER, H .
JOURNAL OF EXPERIMENTAL MEDICINE, 1988, 167 (05) :1697-1707
[10]
MOLECULAR AND BIOLOGICAL CHARACTERIZATION OF A LIGAND FOR CD27 DEFINES A NEW FAMILY OF CYTOKINES WITH HOMOLOGY TO TUMOR-NECROSIS-FACTOR [J].
GOODWIN, RG ;
ALDERSON, MR ;
SMITH, CA ;
ARMITAGE, RJ ;
VANDENBOS, T ;
JERZY, R ;
TOUGH, TW ;
SCHOENBORN, MA ;
DAVISSMITH, T ;
HENNEN, K ;
FALK, B ;
COSMAN, D ;
BAKER, E ;
SUTHERLAND, GR ;
GRABSTEIN, KH ;
FARRAH, T ;
GIRI, JG ;
PATRICIABECKMANN, M .
CELL, 1993, 73 (03) :447-456