T-bet (TBX21) is a transcription factor required for the optimal development of type 1 immune responses. Although initially characterized for its intrinsic role in T cell functional polarization, endogenous T-bet may also be critical to the licensing of type 1-biasing APCs. Here, we investigated whether human dendritic cells (DC) genetically engineered to express high levels of T-bet (ie, DC. Tbet) promote superior type 1 T cell responses in vitro. We observed that DC. Tbet were selective activators of type 1 effector T cells developed from the naive pool of responder cells, whereas DC. Tbet and control DC promoted type 1 responses equitably from the memory pool of responder cells. Naive T cells primed by (staphylococcal enterotoxin B or tumor-associated protein-loaded) DC. Tbet exhibited an enhancement in type 1-and a concomitant reduction in Th2-and regulatory T cell-associated phenotype/function. Surprisingly, DC. Tbets were impaired in their production of IL-12 family member cytokines (IL-12p70, IL-23, and IL-27) when compared with control DC, and the capacity of DC. Tbet to preferentially prime type 1 T cell responses was only minimally inhibited by cytokine (IL-12p70, IL-23, IFN-γ) neutralization or receptor (IL-12Rβ2, IL-27R) blockade during T cell priming. The results of transwell assays suggested the DC. Tbet-mediated effects are predominantly the result of direct DC-T cell contact or their close proximity, thereby implicating a novel, IL-12-independent mechanism by which DC. Tbets promote improved type 1 functional polarization from naive T cell responders. Given their superior type 1 polarizing capacity, DC. Tbet may be suitable for use in vaccines designed to prevent/treat cancer or infectious disease.