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宿主与病毒对RIG-I介导的抗病毒免疫的调节

Host and Viral Modulation of RIG-I-Mediated Antiviral Immunity.

作者信息

Liu Yiliu, Olagnier David, Lin Rongtuan

机构信息

Jewish General Hospital, Lady Davis Institute, McGill University, Montreal, QC, Canada; Division of Experimental Medicine, McGill University, Montreal, QC, Canada.

Jewish General Hospital, Lady Davis Institute, McGill University, Montreal, QC, Canada; Division of Experimental Medicine, McGill University, Montreal, QC, Canada; Department of Microbiology and Immunology, McGill University, Montreal, QC, Canada.

出版信息

Front Immunol. 2017 Jan 3;7:662. doi: 10.3389/fimmu.2016.00662. eCollection 2016.

DOI:10.3389/fimmu.2016.00662
PMID:28096803
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5206486/
Abstract

Innate immunity is the first line of defense against invading pathogens. Rapid and efficient detection of pathogen-associated molecular patterns pattern-recognition receptors is essential for the host to mount defensive and protective responses. Retinoic acid-inducible gene-I (RIG-I) is critical in triggering antiviral and inflammatory responses for the control of viral replication in response to cytoplasmic virus-specific RNA structures. Upon viral RNA recognition, RIG-I recruits the mitochondrial adaptor protein mitochondrial antiviral signaling protein, which leads to a signaling cascade that coordinates the induction of type I interferons (IFNs), as well as a large variety of antiviral interferon-stimulated genes. The RIG-I activation is tightly regulated various posttranslational modifications for the prevention of aberrant innate immune signaling. By contrast, viruses have evolved mechanisms of evasion, such as sequestrating viral structures from RIG-I detections and targeting receptor or signaling molecules for degradation. These virus-host interactions have broadened our understanding of viral pathogenesis and provided insights into the function of the RIG-I pathway. In this review, we summarize the recent advances regarding RIG-I pathogen recognition and signaling transduction, cell-intrinsic control of RIG-I activation, and the viral antagonism of RIG-I signaling.

摘要

固有免疫是抵御入侵病原体的第一道防线。快速且高效地检测病原体相关分子模式及模式识别受体对于宿主启动防御和保护反应至关重要。视黄酸诱导基因I(RIG-I)在触发抗病毒和炎症反应以控制细胞质中病毒特异性RNA结构的病毒复制方面起着关键作用。在识别病毒RNA后,RIG-I招募线粒体适配蛋白线粒体抗病毒信号蛋白,这会引发一个信号级联反应,该反应协调I型干扰素(IFN)的诱导以及多种抗病毒干扰素刺激基因的表达。RIG-I的激活受到多种翻译后修饰的严格调控,以防止异常的固有免疫信号传导。相比之下,病毒已经进化出逃避机制,例如将病毒结构与RIG-I的检测隔离开来,以及靶向受体或信号分子进行降解。这些病毒与宿主的相互作用拓宽了我们对病毒发病机制的理解,并为RIG-I通路的功能提供了见解。在本综述中,我们总结了关于RIG-I病原体识别和信号转导、RIG-I激活的细胞内在控制以及RIG-I信号的病毒拮抗作用的最新进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2986/5206486/a4bef28263d4/fimmu-07-00662-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2986/5206486/3659a4abed94/fimmu-07-00662-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2986/5206486/01f5fd59316f/fimmu-07-00662-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2986/5206486/a4bef28263d4/fimmu-07-00662-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2986/5206486/3659a4abed94/fimmu-07-00662-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2986/5206486/01f5fd59316f/fimmu-07-00662-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2986/5206486/a4bef28263d4/fimmu-07-00662-g003.jpg

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