Staying alive: cell death in antiviral immunity.

Staying alive: cell death in antiviral immunity.
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DOI:
10.1016/j.molcel.2014.01.027
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发表时间:
2014-04-24
期刊:
影响因子:
16
通讯作者:
Chan, Francis Ka-Ming
Chan, Francis Ka-Ming
中科院分区:
生物学1区
文献类型:
--
作者:
Upton, Jason W.;Chan, Francis Ka-Ming

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细胞程序性死亡是宿主防御入侵细胞内病原体的一个组成部分。细胞凋亡、程序性坏死和焦亡各自用于限制感染细胞中的病原体复制,同时促进形成有效的长期宿主免疫的炎症和先天性应答。仔细调节细胞死亡的重要性在由这些途径的缺陷引起的炎症和自身免疫性疾病谱中是显而易见的。此外,许多病毒编码程序性细胞死亡的抑制剂,以在感染期间破坏这些宿主反应,从而促进其自身的复制和持久性。因此,由于病毒和细胞都在争夺这些途径的控制权,生存之战形成了复杂的宿主-病原体相互作用。本文将讨论程序性细胞死亡在维持免疫系统中的多方面作用及其在宿主防御中的关键功能,特别强调病毒感染。
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 programmed cell death plays in maintaining the immune system and its critical function in host defense, with a special emphasis on viral infections.
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