a, IL‐1β counteracted Th17 plasticity. IL‐17A MFI in Th17 (CD4+ Foxp3RFP– IL‐17AKatushka+ YFP+/– IL‐10eGFP+/–) differentiated in the presence of TGF‐β1, IL‐6, IL‐23 or IL‐1β, IL‐6, IL‐23. One experiment out of five is shown. Two technical replicates are reported. b, Dose‐response effect of TGF‐β1 on the induction of Tr1exTh17 cells cultured in the presence of IL‐6, IL‐23, IL‐1β. In the last conditions we added anti‐TGF‐β1 monoclonal antibody. TGF‐β1 was diluted 1:2 starting from the concentration of 4 ng ml−1. One experiment out of five is shown. Two technical replicates are reported. c, In line with the literature29, Smad3 chemical inhibition also favours Th17 cell development. Frequency of Th17 cells cultured in the presence or in the absence Smad3 inhibitor at the indicated different concentrations of TGF‐β1 (4–0.25 ng ml−1). One experiment out of five is shown. Three technical replicates are reported. d, mRNA expression of Ahr in CD4 T cells cultured in the presence of either TGF‐β1, IL‐6, IL‐23 or IL‐1β, IL‐6, IL‐23. The expression is normalized to HPRT. One experiment out of two is shown. Two technical replicates are reported. e, Tr1exTh17 cells were polarized in vitro in the presence of TGF‐β1+IL‐6+IL‐23+FICZ and transferred into Rag1−/− mice ± (p)TH17 cells. Endoscopic colitis score and percentage of initial body weight in the indicated groups are shown. Each dot represents one mouse. Results are cumulative from three independent experiments. Mean and s.e.m., *P ≤ 0.05 by Mann–Whitney U‐-test, two‐tailed. f, Th17 cells were isolated from the intestine of anti‐CD3 monoclonal antibody and then restimulated in vitro in the presence of either anti‐TGF‐β+IL‐6 or IL‐6+TGF‐β1+FICZ for 5 days. Frequencies of Tr1exTh17 cells among total cells (left) and among exTh17 cells (right) are reported. Results are cumulative from three independent experiments. Each dot represents a pool of Th17 cells isolated from five mice treated with anti‐CD3. Mean and s.e.m., *P ≤ 0.05, by Mann–Whitney U‐-test, two tailed.