RIG-I-like receptor regulation in virus infection and immunity.
RIG-I-like receptor regulation in virus infection and immunity.
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DOI：
10.1016/j.coviro.2015.01.004
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发表时间：
2015-06
影响因子：
5.9
通讯作者：
Gack, Michaela U.
中科院分区：
文献类型：
--
作者：
Chan, Ying Kai;Gack, Michaela U.
磷酸化和K63连接的泛素化的平衡调节RIG-I。RIG-I和MAVS功能通过选择性剪接和翻译来调节。亚细胞定位和自噬调节RLR信号传导。病毒病原体操纵RLR-MAVS激活的调节步骤。哺乳动物细胞具有检测病毒病原体和启动抗病毒应答的内在能力，其特征在于干扰素（IFN）和促炎细胞因子的诱导。需要对导致细胞因子产生的信号传导途径进行精细调节，以确保有效清除病毒，同时防止由过量细胞因子释放引起的组织损伤。在这里，我们专注于调节RIG-I样受体（RLRs）及其衔接蛋白MAVS，宿主机器的关键组成部分感应外来RNA触发的信号转导的机制。具体来说，我们总结了最近的进展，了解RLR信号是如何调节的翻译后和转录后机制，microRNA（miRNA）和自噬。我们进一步讨论了病毒如何靶向这些免疫逃避的调节机制。
A balance of phosphorylation and K63-linked ubiquitination regulates RIG-I. RIG-I and MAVS functions are modulated by alternative splicing and translation. Subcellular localization and autophagy regulate RLR signaling. Viral pathogens manipulate the regulatory steps of RLR–MAVS activation. 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.
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