Abstract
Abstract The Th17 cells utilize the retinoid-related orphan receptor-γ (Rorg) gene to specify their differentiation and lineage-specific function. However, how Rorg is switched on during Th17 differentiation is unknown. We report here that the transcription factor c-Rel drives Th17 differentiation by binding to, and activating, two distinct Rorg promoters that control RORγT and RORγ expression, respectively. Similar to RORγT, RORγ is selectively expressed in Th17 cells and is effective in specifying the Th17 phenotype. c-Rel-deficient T cells are significantly compromised in Th17 differentiation, and c-Rel-deficient mice are defective in Th17 responses, and resistant to autoimmune diseases. Thus, Th17 immunity is controlled by a c-Rel−RORγ−RORγT axis, and strategies targeting Rel/NF-κB can be effective for controlling Th17 cell-mediated diseases.
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