Staying Alive: Cell Death in Antiviral Immunity

被引:123
|
作者
Upton, Jason W. [1 ]
Chan, Francis Ka-Ming [2 ]
机构
[1] Univ Texas Austin, Inst Cellular & Mol Biol, Dept Mol Biosci, Austin, TX 78712 USA
[2] Univ Massachusetts, Sch Med, Dept Pathol, Worcester, MA 01605 USA
关键词
RECEPTOR-INTERACTING PROTEIN; TUMOR-NECROSIS-FACTOR; MIXED LINEAGE KINASE; CYTOCHROME-C RELEASE; PROGRAMMED NECROSIS; DOMAIN-LIKE; GRANZYME-B; MEDIATED APOPTOSIS; MOLECULAR SWITCH; FAS LIGAND;
D O I
10.1016/j.molcel.2014.01.027
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Programmed cell death is an integral part of host defense against invading intracellular pathogens. Apoptosis, programmed necrosis, and pyroptosis each serve to limit pathogen replication in infected cells, while simultaneously promoting the inflammatory and innate responses that shape effective long-term host immunity. The importance of carefully regulated cell death is evident in the spectrum of inflammatory and autoimmune disorders caused by defects in these pathways. Moreover, many viruses encode inhibitors of programmed cell death to subvert these host responses during infection, thereby facilitating their own replication and persistence. Thus, as both virus and cell vie for control of these pathways, the battle for survival has shaped a complex host-pathogen interaction. This review will discuss the multifaceted role that programmed cell death plays in maintaining the immune system and its critical function in host defense, with a special emphasis on viral infections.
引用
收藏
页码:273 / 280
页数:8
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