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论文题目:	Role of Itk signalling in the interaction between influenza A virus and T-cells
作者:	Fan, KW; Jia, YP; Wang, S; Li, H; Wu, DF; Wang, GS; Chen, JL
联系作者:	Chen, JL
刊物名称:	JOURNAL OF GENERAL VIROLOGY
期:
卷:	93
页:	987-997
年份:	2012
影响因子:	3.363
论文下载:	下载地址
摘要:	Although the T-cell-mediated immune response to influenza virus has been studied extensively, little information is available on the direct interaction between influenza virus and T-cells that pertains to severe diseases in humans and animals. To address these issues, we utilized the BALB/c mouse model combined with primary T-cells infected with A/WSN/33 influenza virus to investigate whether influenza virus has an affinity for T-cells in vivo. We observed that small proportions of CD4(+) T-cells and CD8(+) T-cells in spleen and thymus expressed viral proteins in infected mice. A significant proportion of mouse primary T-cells displayed expression of alpha-2,6 sialic acid-linked influenza virus receptor and were infected directly by influenza A virus. These experiments reveal that there exists a population of T-cells that is susceptible to influenza A virus infection. Furthermore, we employed human Jurkat T-cells to investigate the virus-T-cell interaction, with particular emphasis on understanding whether Itk (interleukin-2-inducible T-cell kinase), a Tec family tyrosine kinase that regulates T-cell activation, is involved in virus infection of T-cells. Interestingly, influenza virus infection resulted in an increased recruitment of Itk to the plasma membrane and an increased level of phospholipase C-gamma 1 (PLC-gamma 1) phosphorylation, suggesting that Itk/PLC-gamma 1 signalling is activated by the virus infection. We demonstrated that depletion of Itk inhibited the replication of influenza A virus, whereas overexpression of Itk increased virus replication. These results indicate that Itk is required for efficient replication of influenza virus in infected T-cells.