Sensing cytoplasmic danger signals by the inflammasome.

Sensing cytoplasmic danger signals by the inflammasome.
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感知炎症体的细胞质危险信号。

DOI:
10.1007/s10875-010-9419-0
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发表时间:
2010-07
影响因子:
9.1
通讯作者:
Alnemri, Emad S.
Alnemri, Emad S.
中科院分区:
医学2区
文献类型:
--
作者:
Alnemri, Emad S.

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先天免疫系统依赖于统称为模式识别受体(PRR)的分子来调查细胞外空间和细胞质中危险病原体、病原体衍生分子或甚至自体衍生分子危险信号的存在,这些危险信号由组织损伤引起。在黑色素瘤2(AIM 2)中缺失的是一种新发现的PRR,其参与检测由DNA病毒感染产生的危险细胞溶质DNA。值得注意的是,最近在AIM 2缺陷小鼠中的研究表明,AIM 2独特地参与感测细胞内细菌土拉弗朗西斯菌的感染,并随后触发caspase-1介导的促炎细胞因子产生和巨噬细胞死亡,从而激活免疫系统的其他组分并消除受感染的巨噬细胞。在这里,我们提供了一个概述,我们目前了解的作用,AIM 2的先天免疫对F。特别是土拉热,以及巨噬细胞感染这种病原体被认为是如何激活AIM 2的。
The innate immune system depends on molecules collectively known as pattern recognition receptors (PRRs) to survey the extracellular space and the cytoplasm for the presence of dangerous pathogens, pathogen-derived molecules, or even self-derived molecular danger signals, which arise from tissue damage. Absent in melanoma 2 (AIM2) is a newly discovered PRR involved in the sensing of dangerous cytosolic DNA produced by infection with DNA viruses. Remarkably, recent studies in AIM2-deficient mice showed that AIM2 is uniquely involved in sensing infection with the intracellular bacteria Francisella tularensis and subsequently triggering caspase-1-mediated pro-inflammatory cytokine production and macrophage cell death, which activate other components of the immune system and eliminate the infected macrophages. Here, we provide an overview of our current understanding of the role of AIM2 in innate immunity against F. tularensis in particular, and how infection of macrophages with this pathogen is thought to activate AIM2.
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发表时间: 2009-03-01
期刊: NATURE IMMUNOLOGY
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