 T-bet deficient lungs infected with sub-lethal dose of influenza virus upregulate Th2 and Th17 responses, leading to increased pulmonary infiltration of neutrophils and eosinophils. This altered inflammatory response did not compromise efficiency in viral clearance or eventual tissue homeostasis, and in fact reduced tissue leakiness following infection. Furthermore, the immune environment resulting from influenza infected T-bet deficient lungs conferred immunity and survival advantage to pneumococcal superinfected hosts. Correspondingly, neutralization of IL-17 or neutrophil depletion by antibody treatment in T-bet-/- hosts reduced pulmonary neutrophil infiltration or antimicrobial peptide expression, reversing immunity against secondary bacterial infection 