Li Kang, Zhong Bo
Department of Immunology, Medical Research Institute, School of Medicine, Wuhan University, Wuhan 430071, China.
Department of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, China.
Immune Netw. 2018 Feb 6;18(1):e4. doi: 10.4110/in.2018.18.e4. eCollection 2018 Feb.
The initiation of cellular antiviral signaling depends on host pattern-recognition receptors (PRRs)-mediated recognition of viral nucleic acids that are known as classical pathogen-associated molecular patterns (PAMPs). PRRs recruit adaptor proteins and kinases to activate transcription factors and epigenetic modifiers to regulate transcription of hundreds of genes, the products of which collaborate to elicit antiviral responses. In addition, PRRs-triggered signaling induces activation of various inflammasomes which leads to the release of IL-1β and inflammation. Recent studies have demonstrated that PRRs-triggered signaling is critically regulated by ubiquitin and ubiquitin-like molecules. In this review, we first summarize an updated understanding of cellular antiviral signaling and virus-induced activation of inflammasome and then focus on the regulation of key components by ubiquitin and ubiquitin-like molecules.
细胞抗病毒信号传导的启动取决于宿主模式识别受体（PRR）介导的对病毒核酸的识别，这些病毒核酸被称为经典的病原体相关分子模式（PAMP）。PRR招募衔接蛋白和激酶以激活转录因子和表观遗传修饰因子，从而调节数百个基因的转录，这些基因的产物协同引发抗病毒反应。此外，PRR触发的信号传导诱导各种炎性小体的激活，从而导致IL-1β的释放和炎症。最近的研究表明，PRR触发的信号传导受到泛素和类泛素分子的严格调控。在本综述中，我们首先总结对细胞抗病毒信号传导和病毒诱导的炎性小体激活的最新认识，然后重点关注泛素和类泛素分子对关键成分的调控。
