inflammasome 的全景：激活机制、细胞死亡与疾病。
A 360° view of the inflammasome: Mechanisms of activation, cell death, and diseases.
机构信息
Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
出版信息
Cell. 2023 May 25;186(11):2288-2312. doi: 10.1016/j.cell.2023.04.025.
Inflammasomes are critical sentinels of the innate immune system that respond to threats to the host through recognition of distinct molecules, known as pathogen- or damage-associated molecular patterns (PAMPs/DAMPs), or disruptions of cellular homeostasis, referred to as homeostasis-altering molecular processes (HAMPs) or effector-triggered immunity (ETI). Several distinct proteins nucleate inflammasomes, including NLRP1, CARD8, NLRP3, NLRP6, NLRC4/NAIP, AIM2, pyrin, and caspases-4/-5/-11. This diverse array of sensors strengthens the inflammasome response through redundancy and plasticity. Here, we present an overview of these pathways, outlining the mechanisms of inflammasome formation, subcellular regulation, and pyroptosis, and discuss the wide-reaching effects of inflammasomes in human disease.
炎症小体是先天免疫系统的关键传感器，通过识别被称为病原体相关分子模式 (PAMPs) 或细胞内稳态破坏的分子（称为内稳态改变分子过程 [HAMPs] 或效应物触发的免疫 [ETI]），对宿主的威胁做出反应。几种不同的蛋白质可引发炎症小体，包括 NLRP1、CARD8、NLRP3、NLRP6、NLRC4/NAIP、AIM2、pyrin 和 caspase-4/-5/-11。这种多样化的传感器通过冗余性和可塑性增强了炎症小体的反应。在这里，我们概述了这些途径，阐述了炎症小体形成、细胞内调节和细胞焦亡的机制，并讨论了炎症小体在人类疾病中的广泛影响。
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