The concentrations of IL-1β and IL-23 were significantly increased at the early stage of infection (Figures 4A,B), suggesting that other innate immune cells infected with influenza virus (alveolar macrophages, dendritic cells, alveolar epithelial cells, etc.)might secret proinflammatory cytokines to promote IL-17 secretion by γδT cells. This evidence concerns the gene IL1B and infection.