Influenza A virus (IAV) infections have been critical issue in public health. Current available vaccines do not offer broad cross-neutralizing antibody against emerging IAV. T dependent-mucosal IgA antibody response in respiratory tract is known to be broadly protective defense system. However, mechanisms of how T cells contribute to the cross-reactive IgA responses remain to be revealed. Here, we demonstrated that the accumulation of TH1 cells in the lung where IAV was primarily replicated was critical for anti-viral IgA responses in the lung. Moreover, our data indicated that IFN-γ from the migrated TH1 cells, but not from TFH cells, has critical role for virus specific IgA responses, because Ifng deficiency resulted in attenuation of IgA responses, but Bcl6 deficiency showed no effect. We also found functional importance of the IL-6 signaling which is vigorously induced in IAV infected lung, for the induction of IgA class-switching B cells based on the results from Il6 deficient mice and B cells specific Stat3 deficient mice. Taken together, these results indicated that the dynamic movement of IFN-γ producing TH1 cells into IL-6 rich micro environment in lung was essential for anti-viral IgA production in respiratory tract.