The strikingly elevated pulmonary IL-27 induced by influenza infection via type I IFN-α/β receptor (IFNAR) signalling pathway predisposed to secondary pneumococcal pneumonia, which was attributable to IL-27-mediated suppression of innate IL-17A production in γδ T cells but not the adaptive Th17-cell response in a STAT1-dependent way, thereby leading to depressed neutrophil response. The gene discussed is IFNAR1; the disease is pneumococcal pneumonia.