SOCS3负调控流感病毒诱导干扰素表达机理的初步研究OA北大核心CSTPCD

[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.