Advance in Post-Translational Modification of RLRs in Antiviral Innate Immunity

维甲酸诱导基因I (Retinoic Acid-Inducible Gene I, RIG-I)样受体(Retinoic Acid Gene I-Like Receptors, RLRs)是病毒感染的关键感受器，能够识别病毒的RNA，激活线粒体抗病毒信号蛋白(Mitochondrial Antiviral Signaling Protein, MAVS)启动下游信号传导，诱导I型干扰素(Interferon, IFN)的产生，建立有效的抗病毒免疫响应。蛋白质翻译后修饰(Post-Translational Modifications, PTMs)作为调控模式识别受体及其下游信号分子稳定性和活性的关键机制，对干扰素介导的免疫反应至关重要。通过不同的PTMs，包括经典的磷酸化和泛素化，以及其他PTMs如甲基化、乙酰化、SUMO化以及ISG化等，不仅影响RLRs自身的功能状态，还影响着其下游信号分子的活性与定位。本文综述了近年来关于RLRs的PTMs在抗病毒免疫方面的研究进展，旨在为挖掘抗病毒治疗的新靶点提供创新思路。Retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs) are RNA sensor molecules, which mediated intracellular virus recognition. Activated RLRs induce downstream signaling via their interactions with mitochondrial antiviral signaling proteins (MAVS), thereby lead to the transcriptional induction of type I interferons (IFN-I) and establish an antiviral host response. Post-translational modification (PTM), as a key mechanism to regulate the activity and stability of pattern recognition receptors and their downstream signaling molecules, plays a critical role in regulating interferon-mediated immune responses. A variety of PTM modifications, including classical phosphorylation and ubiquitination, as well as methylation, acetylation, SUMOylation, and ISGylation, not only affect the functional status of RLRs, but also the activity and localization of their downstream signaling molecules. This paper reviews the PTM regulation of RLRs in antiviral immunity in recent years, aiming to provide new insights of innate immunity and antiviral therapy.