IL‐9 is a pleiotropic cytokine with key functions in tolerance and inflammation, and its expression is considered a hallmark of Th2‐lineage cells. Here, we report that human and mouse Th17 cells are a significant source of IL‐9. The expression of IL‐9 by Th17 cells was strictly dependent on the presence of TGF‐β and IL‐1β, and inhibited by IL‐4. IL‐9‐deficient Th17 cells induced more severe autoimmune gastritis following transfer to nu/nu recipient mice. Th17 cells did not appear to be the target of IL‐9 bioactivity as Th17 expansion and differentiation was comparable using IL‐9‐deficient CD4⁺ cells or when IL‐9 was neutralized with antibodies in vitro. However, reduced mast cell activity was associated with the increased pathogenicity of IL‐9‐deficient Th17 cells. Together, these results demonstrate a previously unappreciated role for IL‐9 in dampening the pathogenic activities of Th17 cells.