Wang Dang, Li Kui
Department of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Viruses. 2025 Jan 7;17(1):72. doi: 10.3390/v17010072.
The tripartite-motif protein 56 (TRIM56) is a RING-type E3 ubiquitin ligase whose functions were recently beginning to be unveiled. While the physiological role(s) of TRIM56 remains unclear, emerging evidence suggests this protein participates in host innate defense mechanisms that guard against viral infections. Interestingly, TRIM56 has been shown to pose a barrier to viruses of distinct families by utilizing its different domains. Apart from exerting direct, restrictive effects on viral propagation, TRIM56 is implicated in regulating innate immune signaling pathways that orchestrate type I interferon response or autophagy, through which it indirectly impacts viral fitness. Remarkably, depending on viral infection settings, TRIM56 either operates in a canonical, E3 ligase-dependent fashion or adopts an enzymatically independent, non-canonical mechanism to bolster innate immune signaling. Moreover, the recent revelation that TRIM56 is an RNA-binding protein sheds new light on its antiviral mechanisms against RNA viruses. This review summarizes recent advances in the emerging roles of TRIM56 in innate antiviral immunity. We focus on its direct virus-restricting effects and its influence on innate immune signaling through two critical pathways: the endolysosome-initiated, double-stranded RNA-sensing TLR3-TRIF pathway and the cytosolic DNA-sensing, cGAS-STING pathway. We discuss the underpinning mechanisms of action and the questions that remain. Further studies understanding the complexity of TRIM56 involvement in innate immunity will add to critical knowledge that could be leveraged for developing antiviral therapeutics.
三聚基序蛋白56(TRIM56)是一种RING型E3泛素连接酶,其功能最近才开始被揭示。虽然TRIM56的生理作用仍不清楚,但新出现的证据表明,这种蛋白质参与了宿主抵御病毒感染的固有防御机制。有趣的是,TRIM56已被证明通过利用其不同结构域对不同病毒家族构成障碍。除了对病毒繁殖产生直接的限制作用外,TRIM56还参与调节协调I型干扰素反应或自噬的固有免疫信号通路,通过该通路间接影响病毒适应性。值得注意的是,根据病毒感染情况,TRIM56要么以典型的、E3连接酶依赖性方式发挥作用,要么采用酶独立的非典型机制来增强固有免疫信号。此外,最近发现TRIM56是一种RNA结合蛋白,这为其针对RNA病毒的抗病毒机制提供了新的线索。本综述总结了TRIM56在固有抗病毒免疫中新兴作用的最新进展。我们重点关注其直接的病毒限制作用以及通过两条关键途径对固有免疫信号的影响:内溶酶体启动的双链RNA感应TLR3-TRIF途径和胞质DNA感应的cGAS-STING途径。我们讨论了其作用的潜在机制以及仍存在的问题。进一步了解TRIM56参与固有免疫复杂性的研究将增加关键知识,可用于开发抗病毒疗法。