Abstract T cells producing IFN-γ have long been considered a stalwart for immune protection against Mycobacterium tuberculosis (Mtb), but their relative importance to pulmonary immunity has been challenged by murine studies that achieved protection by adoptively transferred Mtb-specific IFN-γ−/− T cells. Using IFN-γ−/− T cell chimeric mice and adoptive transfer of IFN-γ−/− T cells into TCRβ−/−δ−/− mice, we demonstrate that control of lung Mtb burden is in fact dependent on T cell–derived IFN-γ, and, furthermore, mice selectively deficient in T cell–derived IFN-γ develop exacerbated disease compared with T cell–deficient control animals, despite equivalent lung bacterial burdens. Deficiency in T cell–derived IFN-γ skews infected and bystander monocyte-derived macrophages to an alternative M2 phenotype and promotes neutrophil and eosinophil influx. Our studies support an important role for T cell–derived IFN-γ in pulmonary immunity against tuberculosis.