T cells differentiate into functionally distinct effector subsets in response to pathogen encounter. Cells of the innate immune system direct this process; CD1d-restricted invariant natural killer T (iNKT) cells, for example, can either promote or inhibit Th ₁ and Th ₂ responses. Recently, a new subset of CD4 ⁺ T helper cells, called Th ₁₇ , was identified that is implicated in mucosal immunity and autoimmune disorders. To investigate the influence of iNKT cells on the differentiation of naïve T cells we used an adoptive transfer model of traceable antigen-specific CD4 ⁺ T cells. Transferred naïve CD25 ⁻ CD62L ⁺ CD4 ⁺ T cells were primed by antigen immunization of the recipient mice, permitting their expansion and Th ₁₇ differentiation. This study establishes that in vivo activation of iNKT cells during T-cell priming impedes the commitment of naïve T cells to the Th ₁₇ lineage. In vivo cytokine neutralization experiments revealed a role for IL-4, IL-10, and IFN-γ in the iNKT-cell-mediated regulation of T-cell lineage development. Moreover, by comparing IL-17 production by antigen-experienced T cells from unmanipulated wild-type mice and iNKT-cell-deficient mice, we demonstrate an enhanced Th ₁₇ response in mice lacking iNKT cells. This invigorated Th ₁₇ response reverts to physiological levels when iNKT cells are introduced into Jα18 ^−/− mice by adoptive transfer, indicating that iNKT cells control the Th ₁₇ compartment at steady state. We conclude that iNKT cells play an important role in limiting development of the Th ₁₇ lineage and suggest that iNKT cells provide a natural barrier against Th ₁₇ responses.