Apoptosis prevention as a mechanism of immune evasion

被引:25
作者
Aubert, M
Jerome, KR
机构
[1] Fred Hutchinson Canc Res Ctr, Program Infect Dis, Seattle, WA 98125 USA
[2] Univ Washington, Dept Lab Med, Seattle, WA 98195 USA
关键词
apoptosis; virus; cytotoxic lymphocyte; antigen presentation; danger signal; innate immunity;
D O I
10.1080/08830180305213
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
When cells are infected with viruses, they may trigger their apoptosis programs. In unicellular organisms, this may have protected cell populations by limiting viral replication from infected cells. Multicellular organisms can also trigger the apoptosis program after viral infection. In response, viruses have evolved a wide variety of inhibitors of apoptosis. In higher organisms, the outcome of viral infections is largely determined by the immune system. Since apoptosis is intimately linked to the function and regulation of the immune system, the ability of viruses to inhibit apoptosis could profoundly alter the immune response. Viral antiapoptotic proteins could protect infected cells from apoptosis induced by cytotoxic lymphocytes, alter antigen cross-presentation and the priming of the immune response, or modulate the expression of danger signals from sites of infection. The virus/host interaction is likely to provide useful lessons regarding the workings of the mammalian immune system.
引用
收藏
页码:361 / 371
页数:11
相关论文
共 75 条
[1]   Dendritic cells acquire antigen from apoptotic cells and induce class I restricted CTLs [J].
Albert, ML ;
Sauter, B ;
Bhardwaj, N .
NATURE, 1998, 392 (6671) :86-89
[2]   The origin of programmed cell death [J].
Ameisen, JC .
SCIENCE, 1996, 272 (5266) :1278-1279
[3]   Adenovirus L4-100K assembly protein is a granzyme B substrate that potently inhibits granzyme B-mediated cell death [J].
Andrade, F ;
Bull, HG ;
Thornberry, NA ;
Ketner, GW ;
Casciola-Rosen, LA ;
Rosen, A .
IMMUNITY, 2001, 14 (06) :751-761
[4]   Incoming human cytomegalovirus pp65 (UL83) contained in apoptotic infected fibroblasts is cross-presented to CD8+ T cells by dendritic cells [J].
Arrode, G ;
Boccaccio, C ;
Lule, J ;
Allart, S ;
Moinard, N ;
Abastado, JP ;
Alam, A ;
Davrinche, C .
JOURNAL OF VIROLOGY, 2000, 74 (21) :10018-10024
[5]   Cross-presentation of human cytomegalovirus pp65 (UL83) to CD8+ T cells is regulated by virus-induced, soluble-mediator-dependent maturation of dendritic cells [J].
Arrode, G ;
Boccaccio, C ;
Abastado, JP ;
Davrinche, C .
JOURNAL OF VIROLOGY, 2002, 76 (01) :142-150
[6]   HSP70 stimulates cytokine production through a CD14-dependant pathway, demonstrating its dual role as a chaperone and cytokine [J].
Asea, A ;
Kraeft, SK ;
Kurt-Jones, EA ;
Stevenson, MA ;
Chen, LB ;
Finberg, RW ;
Koo, GC ;
Calderwood, SK .
NATURE MEDICINE, 2000, 6 (04) :435-442
[7]   Modulation of apoptosis during herpes simplex virus infection in human cells [J].
Aubert, M ;
Blaho, JA .
MICROBES AND INFECTION, 2001, 3 (10) :859-866
[8]   Dendritic cells and the control of immunity [J].
Banchereau, J ;
Steinman, RM .
NATURE, 1998, 392 (6673) :245-252
[9]   Reovirus receptors and apoptosis [J].
Barton, ES ;
Chappell, JD ;
Connolly, JL ;
Forrest, JC ;
Dermody, TS .
VIROLOGY, 2001, 290 (02) :173-180
[10]   Necrotic but not apoptotic cell death releases heat shock proteins, which deliver a partial maturation signal to dendritic cells and activate the NF-κB pathway [J].
Basu, S ;
Binder, RJ ;
Suto, R ;
Anderson, KM ;
Srivastava, PK .
INTERNATIONAL IMMUNOLOGY, 2000, 12 (11) :1539-1546