Cytotoxic lymphocytes and cardiac electrophysiology

被引:29
作者
Binah, O [1 ]
机构
[1] Technion Israel Inst Technol, Bernard Katz Minerva Ctr Cell Biophys, Bruce Rappaport Fac Med, Rappaport Family Inst Res Med Sci, IL-31096 Haifa, Israel
关键词
cytotoxic lymphocytes; ventricular myocytes; perforin/granzymes; Fas receptor; 1,4,5-inositol triphosphate;
D O I
10.1006/jmcc.2002.2056
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
It is widely recognized that immune effector mechanisms contribute to cardiac dysfunction in major cardiac pathologies. such as myocarditis and the consequent dilated cardiomyopathy, Chagas' disease and heart transplant rejection. Of the wealth of immune mechanisms known to affect cardiac function. this review will deal with the adverse effects caused by cytotoxic T lymphocytes (CTL. CD4(+) and CD8(+) T lymphocytes). which participate in a broad range of heart pathologies. The interaction between cytotoxic lymphocytes and their target cells can set off two different effector mechanisms: (1) The perforin/granzymes, and (2) The Fas/FasL. In this review, I will discuss these mechanisms, and present experimental evidence showing that both can adversely affect cardiac myocytes in vitro, in a way that can contribute to a decline in the overall cardiac function. (C) 2002 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:1147 / 1161
页数:15
相关论文
共 74 条
[11]  
Binah O, 2000, INT J MOL MED, V6, P3
[12]  
Browne KA, 1999, MOL CELL BIOL, V19, P8604
[13]  
CAMPBELL DL, 1993, J GEN PHYSIOL, V101, P571, DOI 10.1085/jgp.101.4.571
[14]   Oxidative stress-mediated cardiac cell death is a major determinant of ventricular dysfunction and failure in dog dilated cardiomyopathy [J].
Cesselli, D ;
Jakoniuk, I ;
Barlucchi, L ;
Beltrami, AP ;
Hintze, TH ;
Nadal-Ginard, B ;
Kajstura, J ;
Leri, A ;
Anversa, P .
CIRCULATION RESEARCH, 2001, 89 (03) :279-286
[15]   EFFECTS OF ALLOIMMUNE INJURY ON CONTRACTION AND RELAXATION IN CULTURED MYOCYTES AND INTACT CARDIAC ALLOGRAFTS [J].
ENSLEY, RD ;
IVES, M ;
ZHAO, LP ;
MCMILLAN, M ;
SHELBY, J ;
BARRY, WH .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1994, 24 (07) :1769-1778
[16]   Fas (CD95/Apo-1)-mediated damage to ventricular myocytes induced by cytotoxic T lymphocytes from perforin-deficient mice - A major role for inositol 1,4,5-trisphosphate [J].
Felzen, B ;
Shilkrut, M ;
Less, H ;
Sarapov, I ;
Maor, G ;
Coleman, R ;
Robinson, RB ;
Berke, G ;
Binah, O .
CIRCULATION RESEARCH, 1998, 82 (04) :438-450
[17]   EFFECTS OF PURIFIED PERFORIN AND GRANZYME-A FROM CYTOTOXIC T-LYMPHOCYTES ON GUINEA-PIG VENTRICULAR MYOCYTES [J].
FELZEN, B ;
BERKE, G ;
ROSEN, D ;
COLEMAN, R ;
TSCHOPP, J ;
YOUNG, JDE ;
BINAH, O .
CARDIOVASCULAR RESEARCH, 1994, 28 (05) :643-649
[18]   The role of TNF in cardiovascular disease [J].
Ferrari, R .
PHARMACOLOGICAL RESEARCH, 1999, 40 (02) :97-105
[19]   Apoptosis in ischemic and reperfused rat myocardium [J].
Fliss, H ;
Gattinger, D .
CIRCULATION RESEARCH, 1996, 79 (05) :949-956
[20]   New paradigm for lymphocyte granule-mediated cytotoxicity - Target cells bind and internalize granzyme B, but an endosomolytic agent is necessary for cytosolic delivery and subsequent apoptosis [J].
Froelich, CJ ;
Orth, K ;
Turbov, J ;
Seth, P ;
Gottlieb, R ;
Babior, B ;
Shah, GM ;
Bleackley, RC ;
Dixit, VM ;
Hanna, W .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (46) :29073-29079