TRIM10是E3连接酶TRIM家族的成员，其基因定位于主要组织相容性复合体I类基因区，与同样定位在此的几个TRIM成员组成一个紧密的基因簇。文献指出，位于该基因簇的TRIM家族成员在天然免疫调节方面发挥着重要作用，但TRIM10能否参与机体的抗病毒免疫还未见报道。我们前期研究发现，敲除TRIM10后，SeV、HSV-60和LPS诱导的IFN-β表达明显受到抑制，并且TRIM10上调MAVS、TRIF和cGAS/STING等调节的IFN-β的转录，随后实验证明，TRIM10与TBK1之间存在相互作用。假设TRIM10是通过E3连接酶活性增强TBK1的激酶活性，进而增强病毒诱导的IFN-β表达。本课题利用免疫共沉淀、报告基因实验以及体外泛素化等实验证明这一假说。本研究旨在阐明TRIM10调控病毒介导I型干扰素表达的分子机制，为细胞调控I型干扰素的产生提供新的认识，为防治病毒感染提供理论基础。

TRIM10 is a member of the E3 ligase TRIM family. Its gene is located in the class I gene region of the main histocompatibility complex. It is closely related to several TRIM members that are also located here. It has been pointed out that the members of TRIM family in this gene cluster play an important role in natural immune regulation, but whether TRIM10 participate in antiviral immunity has not been reported. In our previous study, we found that after knocking out TRIM10, the expression of IFN-β induced by SeV, HSV-60 and LPS was significantly inhibited, and TRIM10 upregulated the transcription of IFN-β regulated by MAVS, TRIF and cGAS/STING. Subsequently, the experiment proved that there was an interaction between TRIM10 and TBK1. It is assumed that TRIM10 enhances the kinase activity of TBK1 through E3 ligase activity, and then enhances IFN-β expression induced by virus. In this study, immunocoprecipitation, reporter gene and ubiquitination in vitro were used to prove the hypothesis. The purpose of this study is to elucidate the molecular mechanism of TRIM10 regulating the expression of type I interferon mediated by virus, provide a new understanding for the production of type I interferon regulated by cells, and provide a theoretical basis for the prevention and control of virus infection.