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BACKGROUND & AIMS Intestinal fibrosis is a significant complication of Crohn's disease (CD). Gut microbiota reactive Th17 cells are crucial in the pathogenesis of CD; however, how Th17 cells induce intestinal fibrosis is still not completely understood. METHODS In this study, T cell transfer model with wild-type (WT) and Areg-/- Th17 cells and dextran sulfate sodium (DSS)-induced chronic colitis model in WT and Areg-/- mice were used. CD4+ T cell expression of Areg was determined by qRT-PCR and ELISA. The effect of Areg on proliferation/migration/collagen expression in human intestinal myofibroblasts was determined. Areg expression was assessed in healthy controls and CD patients with or without intestinal fibrosis. RESULTS Although Th1 and Th17 cells induced intestinal inflammation at similar levels when transferred into Tcrβxδ-/- mice, Th17 cells induced more severe intestinal fibrosis. Th17 cells expressed higher levels of Areg than Th1 cells. Areg-/- mice developed less severe intestinal fibrosis compared with WT mice upon DSS insults. Transfer of Areg-/- Th17 cells induced less severe fibrosis in Tcrβxδ-/- mice compared with WT Th17 cells. IL-6 and IL-21 promoted Areg expression in Th17 cells by activating Stat3. Stat3 inhibitor suppressed Th17-induced intestinal fibrosis. Areg promoted human intestinal myofibroblast proliferation, motility, and collagen I expression, which was mediated by activating mTOR and MEK. Areg expression was increased in intestinal CD4+ T cells in fibrotic sites compared with non-fibrotic sites from CD patients. CONCLUSIONS These findings reveal that Th17-derived Areg promotes intestinal fibrotic responses in experimental colitis and human CD patients. Thereby, Areg might, serve as a potential therapeutic target for fibrosis in CD.