The TRIM25 Gene in Ducks: Cloning, Characterization and Antiviral Immune Response

文献类型： 外文期刊

第一作者： Liu, Jinlu

作者： Liu, Jinlu;Chen, Jianzhou;Luo, Shuwen;Dong, Xiaoqian;Zheng, Ming;Chen, Guohong;Xu, Qi;Gu, Tiantian

作者机构：

关键词： duck; TRIM25; IFN-beta; innate immune

期刊名称：GENES （ 影响因子：4.141； 五年影响因子：4.474 ）

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年卷期： 2022 年 13 卷 11 期

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收录情况： SCI

摘要： Simple SummaryTRIM25, as an important member of the TRIM family, has been frequently demonstrated in regulating the host's antiviral response by activating innate immunity. Ducks are a natural reservoir and often serve as asymptomatic carriers of influenza A viruses, but the beneficial roles of TRIM25 in modulating the immune response remain largely unknown in ducks. On this basis, this study characterized duTRIM25 and explored the role of different domains of duTRIM25 in duck antiviral immune response. The results displayed that the overexpression of duTRIM25 resulted in the IFN-beta production after 5 & PRIME;ppp dsRNA infection and the SPRY domain of duTRIM25 partially enhanced duTRIM25's antiviral activity. These data might reveal the functions of duTRIM25 in antiviral infections, providing new insights for understanding the protective immune responses of ducks.TRIM25, as a significant member of the TRIM family, has been frequently demonstrated in regulating the host's antiviral response by activating innate immunity. Ducks are often asymptomatic carriers of influenza A viruses, but the beneficial roles of TRIM25 in modulating the immune response remain largely unknown in ducks. In this study, we characterized the TRIM25, which contains a 16 bp 5 & PRIME;-UTR, a 279 bp 3 & PRIME;-UTR and a 2052 bp ORF that encodes 683 amino acid residues. In addition, we found that duTRIM25 transcripts were widely expressed in the 10 tissues tested, with higher expression levels in the kidney, liver, muscle and spleen and lower expression levels in the duodenum and blood. In addition, the six kinds of virus- or bacteria-mimicking stimuli were transfected into DEFs, and duTRIM25 was induced significantly with 5 & PRIME;ppp dsRNA stimulation. Furthermore, overexpression of duTRIM25 followed by treatment with 5 & PRIME;ppp dsRNA resulted in an increase in IFN-beta. The SPRY domain of duTRIM25 contributed to promoting IFN-beta activity in DEFs challenged with 5 & PRIME;ppp dsRNA. Taken together, our findings suggest that duck TRIM25 can induce the production of IFN-beta against double-stranded RNA virus stimuli and that the SPRY domain of duTRIM25 was critical for the infection.

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