Inflammasomes and host defenses against bacterial infections.

Inflammasomes and host defenses against bacterial infections.
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DOI:
10.1016/j.mib.2012.11.008
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发表时间:
2013-02
影响因子:
5.4
通讯作者:
Lien E
Lien E
中科院分区:
生物学2区
文献类型:
--
作者:
Vladimer GI;Marty-Roix R;Ghosh S;Weng D;Lien E

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炎性小体是一种重要的分子蛋白复合物,它能将IL-1β和IL-18蛋白水解为成熟的炎性细胞因子。此外,炎性小体启动可能独立于这些细胞因子的热凋亡细胞死亡。炎性小体是引发针对许多病原体的先天免疫应答的核心,并且是细菌感染后诱导宿主防御的关键组分。本文综述了NLRP 1、NLRP 3、NLRC 4、NLRP 6、NLRP 7、NLRP 12和AIM 2介导的细菌识别相关的最新发现。现在认为炎性小体活化和调节的机制涉及激酶如PKR和PKCδ,配体结合蛋白如NAIP,以及除了半胱天冬酶-1之外的半胱天冬酶-11和半胱天冬酶-8。未来的研究将确定特定的炎性体成分如何配对以最佳地应对特定的细菌。
The inflammasome has emerged as an important molecular protein complex which initiates proteolytic processing of pro-IL-1β and IL-18 into mature inflammatory cytokines. In addition, inflammasomes initiate pyroptotic cell death that may be independent of those cytokines. Inflammasomes are central to elicit innate immune responses against many pathogens, and are key components in the induction of host defenses following bacterial infection. Here, we review recent discoveries related to NLRP1, NLRP3, NLRC4, NLRP6, NLRP7, NLRP12 and AIM2-mediated recognition of bacteria. Mechanisms for inflammasome activation and regulation are now suggested to involve kinases such as PKR and PKCδ, ligand binding proteins such as the NAIPs, and caspase-11 and caspase-8 in addition to caspase-1. Future research will determine how specific inflammasome components pair up in optimal responses to specific bacteria.
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