Necroptosis in anti-viral inflammation.

Necroptosis in anti-viral inflammation.
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DOI:
10.1038/s41418-018-0172-x
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发表时间:
2019-01
影响因子:
12.4
通讯作者:
Chan FK
Chan FK
中科院分区:
生物学1区
文献类型:
--
作者:
Nailwal H;Chan FK

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免疫系统的主要功能是保护宿主免受入侵病原体的侵害。作为回应,微生物病原体已经开发出各种策略来逃避免疫系统的检测和破坏。宿主和病原体之间的拔河是塑造生物进化的强大力量。调节性细胞死亡(RCD)是限制细胞内病原体如病毒的储存库的宿主反应。由于病原体特异性T细胞和B细胞应答通常需要几天时间,因此发展缓慢,因此在感染的最初几天内受感染细胞的RCD对于生物体存活至关重要。这种先天性免疫应答不仅限制病毒复制,而且还通过细胞死亡相关的损伤相关分子模式(DAMP)的释放来促进抗病毒炎症。近年来,坏死性凋亡已被认为是对许多病毒的重要反应。坏死性凋亡的中心适配器RIPK3也通过细胞死亡非依赖性活性(例如促进细胞因子基因表达)发挥抗病毒作用。在这里,我们将讨论病毒如何抵消这种宿主防御机制的最新进展,以及坏死性凋亡对抗病毒炎症反应的影响。坏死性凋亡促进抗病毒炎症,这是由病毒编码的抑制剂反击。
The primary function of the immune system is to protect the host from invading pathogens. In response, microbial pathogens have developed various strategies to evade detection and destruction by the immune system. This tug-of-war between the host and the pathogen is a powerful force that shapes organismal evolution. Regulated cell death (RCD) is a host response that limits the reservoir for intracellular pathogens such as viruses. Since pathogen-specific T cell and B cell responses typically take several days and is therefore slow-developing, RCD of infected cells during the first few days of the infection is critical for organismal survival. This innate immune response not only restricts viral replication, but also serves to promote anti-viral inflammation through cell death-associated release of damage-associated molecular patterns (DAMPs). In recent years, necroptosis has been recognized as an important response against many viruses. The central adaptor for necroptosis, RIPK3, also exerts anti-viral effects through cell death-independent activities such as promoting cytokine gene expression. Here, we will discuss recent advances on how viruses counteract this host defense mechanism and the effect of necroptosis on the anti-viral inflammatory reaction. Necroptosis facilitates anti-viral inflammation, which is countered by virally-encoded inhibitors.
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