Nevertheless, in wild-type mice, the detrimental effect of type I IFNs induced during primary nonlethal influenza infection on increased susceptibility to secondary Streptococcus pneumonia infection by negative regulation of lung γδ T cell-mediated IL-17 production and IL-17-induced neutrophil recruitment, involving in lung immunity to bacterial infection, has been reported [112]. The gene discussed is IL17A; the disease is bacterial infectious disease.