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通过先天免疫感应核酸检测微生物感染

Detection of Microbial Infections Through Innate Immune Sensing of Nucleic Acids.

机构信息

Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9148, USA; email:

Center for Inflammation Research, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.

出版信息

Annu Rev Microbiol. 2018 Sep 8;72:447-478. doi: 10.1146/annurev-micro-102215-095605.

Abstract

Microbial infections are recognized by the innate immune system through germline-encoded pattern recognition receptors (PRRs). As most microbial pathogens contain DNA and/or RNA during their life cycle, nucleic acid sensing has evolved as an essential strategy for host innate immune defense. Pathogen-derived nucleic acids with distinct features are recognized by specific host PRRs localized in endolysosomes and the cytosol. Activation of these PRRs triggers signaling cascades that culminate in the production of type I interferons and proinflammatory cytokines, leading to induction of an antimicrobial state, activation of adaptive immunity, and eventual clearance of the infection. Here, we review recent progress in innate immune recognition of nucleic acids upon microbial infection, including pathways involving endosomal Toll-like receptors, cytosolic RNA sensors, and cytosolic DNA sensors. We also discuss the mechanisms by which infectious microbes counteract host nucleic acid sensing to evade immune surveillance.

摘要

微生物感染通过种系编码的模式识别受体 (PRRs) 被先天免疫系统识别。由于大多数微生物病原体在其生命周期中含有 DNA 和/或 RNA,因此核酸感应已成为宿主先天免疫防御的重要策略。具有独特特征的病原体衍生核酸被定位在内体和细胞质中的特定宿主 PRRs 识别。这些 PRRs 的激活引发信号级联反应,最终导致 I 型干扰素和促炎细胞因子的产生,导致抗菌状态的诱导、适应性免疫的激活和感染的最终清除。在这里,我们综述了微生物感染后先天免疫识别核酸的最新进展,包括涉及内体 Toll 样受体、细胞质 RNA 传感器和细胞质 DNA 传感器的途径。我们还讨论了传染性微生物对抗宿主核酸感应以逃避免疫监视的机制。

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