Host and Viral Modulation of RIG-I-Mediated Antiviral Immunity.
Host and Viral Modulation of RIG-I-Mediated Antiviral Immunity.
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DOI：
10.3389/fimmu.2016.00662
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发表时间：
2016
影响因子：
7.3
通讯作者：
Lin R
中科院分区：
文献类型：
--
作者：
Liu Y;Olagnier D;Lin R
先天免疫是抵抗病原体入侵的第一道防线。通过模式识别受体快速有效地检测病原体相关的分子模式对于宿主进行防御和保护反应至关重要。视黄酸诱导基因-I（RIG-I）在响应细胞质病毒特异性RNA结构而触发用于控制病毒复制的抗病毒和炎症反应中是至关重要的。在病毒RNA识别后，RIG-I募集线粒体接头蛋白线粒体抗病毒信号蛋白，其导致协调I型干扰素（IFN）以及多种抗病毒干扰素刺激基因的诱导的信号级联。RIG-I激活通过各种翻译后修饰进行严格调节，以防止异常的先天免疫信号传导。相比之下，病毒已经进化出逃避机制，例如从RIG-I检测中隔离病毒结构，并靶向受体或信号分子进行降解。这些病毒-宿主相互作用拓宽了我们对病毒发病机制的理解，并提供了对RIG-I途径功能的见解。本文就RIG-I的病原体识别和信号转导、RIG-I激活的细胞内调控以及RIG-I信号转导的病毒拮抗作用等方面的最新研究进展进行综述。
Innate immunity is the first line of defense against invading pathogens. Rapid and efficient detection of pathogen-associated molecular patterns via 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 via 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.
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影响因子：
56.9
作者：
Choudhary, Chunaram;Kumar, Chanchal;Mann, Matthias
通讯作者：
Mann, Matthias
影响因子：
6.4
作者：
Dalrymple NA;Cimica V;Mackow ER
通讯作者：
Mackow ER
SARS冠状病毒木瓜蛋白酶样蛋白酶通过与STING-TRAF3-TBK1复合物相互作用抑制I型干扰素信号通路
影响因子：
21.1
作者：
Chen, Xiaojuan;Yang, Xingxing;Zheng, Yang;Yang, Yudong;Xing, Yaling;Chen, Zhongbin
通讯作者：
Chen, Zhongbin
影响因子：
5.4
作者：
Best, SM;Morris, KL;Bloom, ME
通讯作者：
Bloom, ME
影响因子：
5.4
作者：
Donelan, NR;Basler, CF;García-Sastre, A
通讯作者：
García-Sastre, A