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病毒感染与免疫中视黄酸诱导基因I样受体的调控

RIG-I-like receptor regulation in virus infection and immunity.

作者信息

Chan Ying Kai, Gack Michaela U

机构信息

Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA.

Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA.

出版信息

Curr Opin Virol. 2015 Jun;12:7-14. doi: 10.1016/j.coviro.2015.01.004. Epub 2015 Jan 30.

Abstract

Mammalian cells have the intrinsic capacity to detect viral pathogens and to initiate an antiviral response that is characterized by the induction of interferons (IFNs) and proinflammatory cytokines. A delicate regulation of the signaling pathways that lead to cytokine production is needed to ensure effective clearance of the virus, while preventing tissue damage caused by excessive cytokine release. Here, we focus on the mechanisms that modulate the signal transduction triggered by RIG-I-like receptors (RLRs) and their adaptor protein MAVS, key components of the host machinery for sensing foreign RNA. Specifically, we summarize recent advances in understanding how RLR signaling is regulated by posttranslational and posttranscriptional mechanisms, microRNAs (miRNAs) and autophagy. We further discuss how viruses target these regulatory mechanisms for immune evasion.

摘要

哺乳动物细胞具有检测病毒病原体并启动抗病毒反应的内在能力,该反应的特征是诱导干扰素(IFN)和促炎细胞因子。需要对导致细胞因子产生的信号通路进行精细调节,以确保有效清除病毒,同时防止因细胞因子过度释放而造成的组织损伤。在这里,我们重点关注调节由视黄酸诱导基因I样受体(RLR)及其接头蛋白线粒体抗病毒信号蛋白(MAVS)触发的信号转导的机制,MAVS是宿主感知外源RNA机制的关键组成部分。具体而言,我们总结了在理解RLR信号如何通过翻译后和转录后机制、微小RNA(miRNA)和自噬进行调控方面的最新进展。我们还将进一步讨论病毒如何针对这些调节机制进行免疫逃逸。

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