Influenza virus infection has the potential to induce excess pulmonary inflammation and massive tissue damage in the infected host. Conventional CD4+ and CD8+ as well as nonconventional innate like T cells respond to infection and make an essential contribution to the clearance of virus infected cells and the resolution of pulmonary inflammation and injury. Emerging evidence in recent years has suggested a critical role of local interactions between lung effector T cells and antigen presenting cells in guiding the accumulation, differentiation and function of effector T cells beyond their initial activation in the draining lymph nodes during influenza infection. As such, lung effector CD4+ and CD8+ T cells utilize multiple effector and regulatory mechanisms to eliminate virus infected cells as well as fine tune the control of pulmonary inflammation and injury. Elucidating the mechanisms by which conventional and nonconventional T cells orchestrate their response in the lung as well as defining the downstream events required for the resolution of influenza infection will be important areas of future basic research which in turn may result in new therapeutic strategies to control the severity of influenza virus infection.
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