福建农业学报2024，Vol.39Issue(2)：131-136,6.DOI:10.19303/j.issn.1008-0384.2024.02.002
SOCS3负调控流感病毒诱导干扰素表达机理的初步研究
A Preliminary Study on Influenza Virus-induced Interferon Regulating Mechanism of SOCS3
摘要
Abstract
[Objective]Regulatory function of the suppressor of cytokine signaling 3(SOCS3)in the interferon signaling pathway during an influenza virus infection on cells was studied.[Method]A549 cell lines were constructed with SOCS3 overexpression by a lentivirus infection and knockdown by siRNA technology.Along with control,they were infected with the influenza virus and sampled at times to assess the expressions and activation of crucial molecules within the interferon signaling pathway using RT-PCR and western blot analysis.[Result]Decreasing expressions of type I interferon IFN-β and type Ⅲ interferons IL-28 and IL-29 were observed following the SOCS3 overexpression in cells.Conversely,the SOCS3 knockdown raised the expressions of IFN-β,IL-28,and IL-29.SOCS3 overexpression also suppressed the expressions of the interferon regulatory factor IRF7 as well as those of the pattern recognition receptors RIG-Ⅰ,MDA5,and TLR3 responsible for detecting influenza virus RNA.The virus induced SOCS3 overexpression inhibited,but the knockdown enhanced,the STAT1 phosphorylation.[Conclusion]An influenza virus invasion on cells induced SOCS3 to recognize the receptors and regulate the mRNA expression inhibiting the type Ⅰ and Ⅲ interferon productions and STAT1 activation resulting in a blockage on the interferon signal transmission.关键词
流感病毒/SOCS3/干扰素/天然免疫/STAT1Key words
Influenza virus/SOCS3/interferon/innate immunity/STAT1分类
农业科技引用本文复制引用
彭本群,胡精蕴,毛亚楠,王淑霖,王佳俊,陈梦颖,尤冬雪,王松..SOCS3负调控流感病毒诱导干扰素表达机理的初步研究[J].福建农业学报,2024,39(2):131-136,6.基金项目
国家自然科学基金项目(U23A20235) （U23A20235）
福建省自然科学基金项目(2020J06016) （2020J06016）
福建农林大学科技创新专项基金(KFb22063XA) （KFb22063XA）
