细胞焦亡可抵御细胞内病原体。
Pyroptotic cell death defends against intracellular pathogens.
作者信息
Jorgensen Ine, Miao Edward A
机构信息
Department of Microbiology and Immunology, Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA; Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
出版信息
Immunol Rev. 2015 May;265(1):130-42. doi: 10.1111/imr.12287.
Abstract
Inflammatory caspases play a central role in innate immunity by responding to cytosolic signals and initiating a twofold response. First, caspase-1 induces the activation and secretion of the two prominent pro-inflammatory cytokines, interleukin-1β (IL-1β) and IL-18. Second, either caspase-1 or caspase-11 can trigger a form of lytic, programmed cell death called pyroptosis. Pyroptosis operates to remove the replication niche of intracellular pathogens, making them susceptible to phagocytosis and killing by a secondary phagocyte. However, aberrant, systemic activation of pyroptosis in vivo may contribute to sepsis. Emphasizing the efficiency of inflammasome detection of microbial infections, many pathogens have evolved to avoid or subvert pyroptosis. This review focuses on molecular and morphological characteristics of pyroptosis and the individual inflammasomes and their contribution to defense against infection in mice and humans.
摘要
炎性半胱天冬酶通过响应胞质信号并引发双重反应，在先天免疫中发挥核心作用。首先，半胱天冬酶-1诱导两种主要促炎细胞因子白细胞介素-1β（IL-1β）和IL-18的激活和分泌。其次，半胱天冬酶-1或半胱天冬酶-11均可触发一种称为细胞焦亡的溶细胞性程序性细胞死亡形式。细胞焦亡的作用是消除细胞内病原体的复制龛，使其易于被次级吞噬细胞吞噬和杀灭。然而，体内细胞焦亡的异常全身性激活可能导致脓毒症。许多病原体已经进化以避免或破坏细胞焦亡，这突出了炎性小体检测微生物感染的效率。本综述重点关注细胞焦亡和各个炎性小体的分子及形态学特征，以及它们在小鼠和人类抗感染防御中的作用。
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