We employed a murine model of pulmonary infection using the intracellular pathogen F. tularensis Live Vaccine Strain (LVS) to investigate the in vivo role of MAIT cells in mucosal immune responses.In the early acute phase of infection, MAIT cells expanded robustly in the lungs, where they preferentially accumulated after reaching their peak expansion in the late phase of infection.  Throughout the course of infection, MAIT cells produced the critical cytokines IFN-γ, TNF-α, and IL-17A.  Importantly, MAIT cells were required for the timely recruitment of IFN-g-producing CD4⁺ and CD8⁺ T cells to the infected lungs, and for control of pulmonary F. tularensis LVS growth.  Similar to other intracellular pathogens, optimal defense against LVS infection requires conventional CD4⁺ and/or CD8⁺ T cells for clearance of the bacterium. We were therefore interested in determining the precise mechanisms by which MAIT cells influence early activation and/or recruitment of conventional T cells.  Here we show that MAIT cell-derived GM-CSF promotes the differentiation of CCR2⁺ inflammatory monocytes into CD11b⁺ dendritic cells in the lungs, and that this early deficit in the development of CD11b⁺ DCs in MR1^-/- mice impairs early CD4⁺ T cell activation.  This study provides in vivo evidence demonstrating that MAIT cells are an important T cell subset with activities that influence both the innate and adaptive phases of mucosal immunity.