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细菌病原体激活和逃避炎症小体。

Inflammasome activation and evasion by bacterial pathogens.

机构信息

Department of Immunology, UConn Health School of Medicine, 263 Farmington Ave, Farmington, CT 06030, USA.

Department of Immunology, UConn Health School of Medicine, 263 Farmington Ave, Farmington, CT 06030, USA.

出版信息

Curr Opin Immunol. 2021 Feb;68:125-133. doi: 10.1016/j.coi.2020.11.006. Epub 2020 Dec 15.

Abstract

Innate immune system plays an essential role in combating infectious diseases by recognizing invading pathogens and activating host defense response. Inflammasomes complexes are a central component of the cytosolic innate immune surveillance and are vital in host defense against bacterial pathogens. Bacterial products or pathogen-induced modifications in the intracellular environment are sensed by the inflammasome receptors that form complexes that serve as a platform for caspase-1-dependent or caspase-11-dependent induction of pyroptosis and secretion of cytokines, IL-1β and IL-18. However, several pathogenic bacteria have developed strategies to evade inflammasome activation. This review highlights the recent advances in the mechanism of inflammasome activation by bacterial pathogens and some of the bacterial evasion strategies of inflammasome activation.

摘要

先天免疫系统通过识别入侵病原体并激活宿主防御反应,在抵御传染病方面发挥着重要作用。炎性小体复合物是细胞溶质固有免疫监视的核心组成部分,对于宿主抵御细菌病原体至关重要。炎性小体受体感知细菌产物或细胞内环境中病原体诱导的修饰,形成复合物,作为依赖半胱天冬酶-1 或依赖半胱天冬酶-11 的细胞焦亡诱导和细胞因子 IL-1β 和 IL-18 分泌的平台。然而,一些致病菌已经发展出逃避炎性小体激活的策略。本综述强调了细菌病原体激活炎性小体的机制的最新进展,以及一些细菌逃避炎性小体激活的策略。

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