TRIM21调控Ⅱ型干扰素信号通路抑制脑心肌炎病毒在RAW264.7巨噬细胞中的增殖OA

[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 sig-nalling 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 repli-cation 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 prolif-eration 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.