Abstract
Abstract Host resistance against influenza A virus infection relies on the efficient collaboration of innate and adaptive immune response. Being a major component of innate immune system, NK cells have been confirmed to limit the replication and spread of influenza virus during early infection. However, their roles in the generation of virus-specific CTLs response still remain exclusive. Consistent with our in vitro study on human NK cells, here we firstly confirmed that murine NK cells could be directly infected with mouse-adaptive influenza A PR8 virus in vivo under both systemic and local infection. However, only systemic infection resulted in severe reduction and dysfunction of spleen NK cells, which was accompanied with the poor antigen-specific killing and IFN-γ secretion rather than the decrease in quantity of CTLs during the acute phase of infection. Importantly, the adoptive transfer of spleen NK cells from mice suffering from local infection rescued the impaired CTLs in systemic influenza virus-infected mice, whereas no similar effects could be observed by using NK cells from healthy mice. Taken together, our results demonstrated that NK cell-mediated help on the generation of functional influenza virus-specific CTLs was infection-dependent and determined by the dose of infection. This study provided some important information for developing novel NK-cell-targeted strategy against severe influenza infection.
Published Version
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