Although tissue resident memory T cells (T RM) in the lung confer robust protection against secondary influenza infection, their in vivo production of IFN-γ is unknown. In this study, using a mouse model, we evaluated production of IFN-γ by influenza-induced T RM (defined as CD103+) that localize to the airways or lung parenchyma. Airway T RM consist of both CD11a hi and CD11a lo populations, with low CD11a expression signifying prolonged airway residence. In vitro, high-dose peptide stimulation evoked IFN-γ from most CD11a hi airway and parenchymal T RM, whereas most CD11a lo airway T RM did not produce IFN-γ. In vivo production of IFN-γ was clearly detectable in CD11a hi airway and parenchymal T RM but essentially absent in CD11a lo airway T RM, irrespective of airway-instilled peptide concentration or influenza reinfection. The majority of IFN-γ–producing airway T RM in vivo were CD11a hi, suggesting recent airway entry. These results question the contribution of long-term CD11a lo airway T RM to influenza immunity and reinforce the importance of defining T RM tissue compartment–specific contributions to protective immunity.