| 摘要: |
| 【 目的】探究TRIM21调控脑心肌炎病毒（EMCV）复制增殖机制与JAK1-STAT1信号通路的关系。 【方法】用Western Blot和RT-qPCR，检测EMCV感染小鼠RAW264.7巨噬细胞后内源性TRIM21的变化；Western Blot、RT-qPCR和TCID50法检测RAW264.7巨噬细胞过表达或敲低表达TRIM21的效果，以及对EMCV复制增殖的影响；半定量PCR和ELISA法检测固有免疫应答中细胞因子的变化；采用半定量PCR和Western Blot法，检测RAW264. 7巨噬细胞过表达或敲低表达TRIM21并感染EMCV后对JAK-STAT信号通路的影响。【结果】EMCV感染RAW264.7巨噬细胞后，内源性TRIM21表达增加，说明TRIM21参与EMCV的复制增殖过程；Western Blot、RT-qPCR和病毒滴度检测结果表明，TRIM21过表达抑制EMCV复制增殖；TRIM21未参与病毒的吸附和侵入过程，但可抑制病毒释放；EMCV感染RAW264.7巨噬细胞后可诱导产生IFN-γ，并促进JAK1、STAT1和IRF9表达。【 结论】TRIM21通过抑制子代病毒释放并诱导RAW264.7巨噬细胞分泌IFN-γ，激活JAK1-STAT1信号通路，以抑制EMCV病毒蛋白的复制增殖。 |
| 关键词: 脑心肌炎病毒 固有免疫应答 TRIM21 IFN-γ |
| DOI：10. 13207/j. jnwafu. 2026. 06. 002 |
| 分类号: |
| 基金项目:甘肃省自然科学基金项目（23JRRA720） |
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| Regulatory effect of TRIM21 on the type Ⅱ interferon signaling pathway to inhibit the proliferation of encephalomyocarditis virus in RAW264.7 cells |
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SHAO Shuai1,2, LIU Mingqi1,2, FAN Yiyang1,2, JI Xiaolan1,2, BAI Jialin3,4,5, LI Qiongyi6,4,5
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1.Engineering Research Centre of Ministry of Education for Key Technology and Industrialisation of Acellular Matrix Vaccine， Northwest Minzu University，Lanzhou，Gansu 730030，China;2.Key Laboratory of Biotechnology and Bioengineering of State Ethnic Affairs Commission， Biomedical Research Center，Northwest Minzu University，Lanzhou，Gansu 730030，China;3.Key Laboratory of Biotechnology and Bioengineering of State Ethnic
Affairs Commission， Biomedical Research Center，Northwest Minzu University，Lanzhou，Gansu 730030，China;4.School of Life Science and Engineering Northwest Minzu University，Lanzhou，Gansu 730030，China;5.Gansu Tech Innovation Center of Animal Cell，Lanzhou，Gansu 730030，China;6.Engineering Research Centre of Ministry of Education for Key Technology and Industrialisation of Acellular Matrix Vaccine，Northwest Minzu University，Lanzhou，Gansu 730030，China
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| Abstract: |
| 【 Objective】This research aims to investigate the relationship between the mechanism by which TRIM21 regulates the replication and proliferation of encephalomyocarditis virus（ EMCV） and JAK1-STAT1 signalling pathway.【Method】Western Blot and RT-qPCR were used to detect the changes of endogenous TRIM21 after the mouse RAW264.7 macrophages were infected by EMCV.Western Blot，RT-qPCR，and TCID50 were used to detect the effects of overexpression or knockdown of TRIM21 and their impact on EMCV replication and proliferation. Semi-quantitative PCR and ELISA were used to detect the changes of cytokines in the intrinsic immune response；semi-quantitative PCR and Western Blot were used to detect the effect of overex?pression or knockdown of TRIM21 in RAW264.7 macrophages infected with EMCV on the JAK-STAT signalling pathway. 【Result】Endogenous TRIM21 expression was upregulated after EMCV infection of RAW264. 7 macrophages，suggesting that TRIM21 was involved in the replication and proliferation process of EMCV. Western Blot，RT-qPCR and viral titre assay showed that TRIM21 overexpression inhibited the replication and proliferation of EMCV. TRIM21 was not involved in the adsorption and invasion process of virus，but it inhibited virus release. EMCV infection of RAW264.7 macrophages induced the production of IFN-γ and promoted the expression of JAK1，STAT1 and IRF9.【Conclusion】TRIM21 inhibited the replication and proliferation of EMCV viral proteins by inhibiting the release of progeny virus and inducing RAW264.7 macrophages to secrete IFN-γ，thereby activating the JAK1-STAT1 signalling pathway. |
| Key words: Encephalomyocarditis virus intrinsic immune response TRIM21 IFN-γ |
