The mechanistic/mammalian target of rapamycin (RAPA) (mTOR) is a key integrative kinase that functions in at least two independent complexes: RAPA-sensitive mTOR complex (C)1 and RAPA-insensitive mTORC2. While mTORC2 in T cells promotes Th2 and Th17 differentiation, its immunologic function in dendritic cells (DC) is largely unknown. We defined the role of rictor, a key mTORC2 component, in myeloid DC and their ability to polarize interacting allogeneic Th cells. When stimulated with TLR ligands, bone marrow-derived DC generated from conditional rictor KOs displayed lower co-inhibitory B7-H1 (CD274) molecule expression, enhanced IL-12p70, IL-23, IL-6 and TNFα production and augmented allogeneic T cell stimulatory ability. Analysis of allopeptide-specific CD4+ T cells after activation by rictor KO DC in vivo revealed significant expansion of IFN-γ+ and IL-17+, but not IL-10+ or CD4+Foxp3+ T cells. These data establish that mTORC2 activity restrains pro-inflammatory responses of conventional DC and their ability to differentiate Th1/Th17 cells.