IL-1 signaling plays a critical role in the early differentiation of Th17 cells. The study shows that IL-1R1 expression in T cells, induced by IL-6, is necessary for Th17-mediated autoimmunity and early Th17 differentiation in vivo. IL-1 signaling in T cells is required for Th17 differentiation mediated by dendritic cells and synergizes with IL-6 and IL-23 to regulate Th17 differentiation and maintain cytokine expression in effector Th17 cells. IL-1 regulates the expression of IRF4 and RORγt during Th17 differentiation, and overexpression of these factors results in IL-1-independent Th17 polarization. The study indicates that IL-1 is critical for Th17 differentiation and may serve as a novel target for Th17-mediated immunopathology. IL-1R1 expression is upregulated in Th17 cells, and its deficiency in T cells impairs Th17 differentiation and leads to reduced IL-17 production. IL-1 signaling is necessary for Th17 responses in vivo, as shown by the reduced severity of EAE in IL-1R1-deficient T cells. IL-1 signaling functions to promote early Th17 differentiation, as demonstrated by the reduced Th17 differentiation in IL-1R1-deficient T cells. IL-1 signaling is also required for the maintenance of Th17 cells in the absence of TCR stimuli. IL-1 signaling regulates Th17 differentiation in the absence of exogenous TGF-β, as shown by the increased Th17 differentiation in the presence of IL-1 and IL-23. IL-1 signaling induces IRF4 and RORγt expression during early Th17 polarization, which is essential for Th17 differentiation. The study highlights the critical role of IL-1 in Th17 differentiation and its potential as a target for immunopathology.IL-1 signaling plays a critical role in the early differentiation of Th17 cells. The study shows that IL-1R1 expression in T cells, induced by IL-6, is necessary for Th17-mediated autoimmunity and early Th17 differentiation in vivo. IL-1 signaling in T cells is required for Th17 differentiation mediated by dendritic cells and synergizes with IL-6 and IL-23 to regulate Th17 differentiation and maintain cytokine expression in effector Th17 cells. IL-1 regulates the expression of IRF4 and RORγt during Th17 differentiation, and overexpression of these factors results in IL-1-independent Th17 polarization. The study indicates that IL-1 is critical for Th17 differentiation and may serve as a novel target for Th17-mediated immunopathology. IL-1R1 expression is upregulated in Th17 cells, and its deficiency in T cells impairs Th17 differentiation and leads to reduced IL-17 production. IL-1 signaling is necessary for Th17 responses in vivo, as shown by the reduced severity of EAE in IL-1R1-deficient T cells. IL-1 signaling functions to promote early Th17 differentiation, as demonstrated by the reduced Th17 differentiation in IL-1R1-deficient T cells. IL-1 signaling is also required for the maintenance of Th17 cells in the absence of TCR stimuli. IL-1 signaling regulates Th17 differentiation in the absence of exogenous TGF-β, as shown by the increased Th17 differentiation in the presence of IL-1 and IL-23. IL-1 signaling induces IRF4 and RORγt expression during early Th17 polarization, which is essential for Th17 differentiation. The study highlights the critical role of IL-1 in Th17 differentiation and its potential as a target for immunopathology.