In this context, our present study unveiled a critical contribution of Th17 cell-derived TGF-β1 to the stability of Th17 cells by demonstrating that (i) autocrine TGF-β1 was required for the expression of latent TGF-β1 on Th17 cells, (ii) TGF-β1-deficient Th17 cells expressed increased levels of Il12rb2 and Il27ra and were more prone to becoming Th1 cells, (iii) TGF-β1-deficient Th17 cells exacerbated autoimmune CNS inflammation and (iv) naïve Tgfb1fl/flIl17aCreR26YFP CD4+ T cells induced more severe experimental colitis than naïve WT CD4+ T cells. This evidence concerns the gene IL12RB2 and colitis.