Our data show that IL-17−/−Mtb HN878-infected lungs accumulate similar numbers of proinflammatory T cells producing IFN-γ, IL-2 and TNF-α, suggest that the increased susceptibility to infection is not due to defects in generation, or accumulation of proinflammatory T cells in the lung, but due to defects in localization of cytokine-producing T cells within lymphoid follicles to mediate macrophage activation. Here, IL2 is linked to infection.