IFN-γ is well known as the signature cytokine of CD4⁺ T helper 1, CD8⁺, and natural killer cells, but recent studies demonstrate that antigen-presenting cells, in particular dendritic cells (DCs), are another potent source for this proinflammatory cytokine. T-bet, a transcription factor that controls IFN-γ expression in CD4⁺ T cells, was reported recently to be expressed in human monocytes and myeloid DCs. In this study we investigate the role of T-bet in this important cell type. The development, differentiation, and activation of bone marrow and splenic DCs were unimpaired in mice lacking T-bet. However, T-bet was essential for the optimal production of IFN-γ by both CD8α⁺ and CD8α^- DCs. T-bet-deficient DCs were significantly impaired in their capacity to secrete IFN-γ after both stimulation with IL-12 alone or in combination with IL-18. Further, T-bet^-/- DCs were impaired in their ability to activate the T helper 1 program of adoptively transferred antigen-specific T cells in vivo. The rapid up-regulation of T-bet by IFN-γ in DCs coupled with a function for DC-derived IFN-γ in T cell activation may constitute a positive feedback loop to maximize type 1 immunity.