先天传感器触发调节细胞死亡以对抗细胞内感染。

IF 26.9 1区 医学 Q1 IMMUNOLOGY
Kengo Nozaki, Lupeng Li, Edward A Miao
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引用次数: 37

摘要

细胞内病原体对动物构成重大威胁。在防御中,先天免疫传感器试图使用模式识别受体来检测这些病原体,这些模式识别受体要么直接检测微生物分子,要么间接检测其致病活性。这些传感器触发不同形式的受调节细胞死亡,包括焦亡、凋亡和坏死亡,它们消除受感染的宿主细胞生态位,同时促进有益的免疫反应。这些防御迫使细胞内病原体进化出最小化或完全逃避传感器的策略。在这篇综述中,我们讨论了驱动细胞死亡的细胞质模式识别受体的最新进展,包括NLRP1、NLRP3、NLRP6、NLRP9、NLRC4、AIM2、IFI16和ZBP1。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Innate Sensors Trigger Regulated Cell Death to Combat Intracellular Infection.

Innate Sensors Trigger Regulated Cell Death to Combat Intracellular Infection.

Innate Sensors Trigger Regulated Cell Death to Combat Intracellular Infection.

Innate Sensors Trigger Regulated Cell Death to Combat Intracellular Infection.

Intracellular pathogens pose a significant threat to animals. In defense, innate immune sensors attempt to detect these pathogens using pattern recognition receptors that either directly detect microbial molecules or indirectly detect their pathogenic activity. These sensors trigger different forms of regulated cell death, including pyroptosis, apoptosis, and necroptosis, which eliminate the infected host cell niche while simultaneously promoting beneficial immune responses. These defenses force intracellular pathogens to evolve strategies to minimize or completely evade the sensors. In this review, we discuss recent advances in our understanding of the cytosolic pattern recognition receptors that drive cell death, including NLRP1, NLRP3, NLRP6, NLRP9, NLRC4, AIM2, IFI16, and ZBP1.

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来源期刊
Annual review of immunology
Annual review of immunology 医学-免疫学
CiteScore
57.20
自引率
0.70%
发文量
29
期刊介绍: The Annual Review of Immunology, in publication since 1983, focuses on basic immune mechanisms and molecular basis of immune diseases in humans. Topics include innate and adaptive immunity; immune cell development and differentiation; immune control of pathogens (viruses, bacteria, parasites) and cancer; and human immunodeficiency and autoimmune diseases. The current volume of this journal has been converted from gated to open access through Annual Reviews' Subscribe to Open program, with all articles published under a CC BY license.
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