Inflammatory bowel disease (IBD) is a chronic inflammatory disease that is thought to arise in part from abnormal adaptive immune responses against intestinal microbiota. T lymphocytes play significant roles in triggering mucosal inflammation and/or maintaining gut immune homeostasis. It has been demonstrated that IL-37 expresses in a variety of cells and exerts a protective function involved in both innate immunity and adaptive immunity. In the present study, a population of IL-37-producing T-cells was detected in the spleen and mesenteric lymph nodes (MLNs) in IL-37^+/+ mice after dextran sodium sulfate (DSS) induction. Adoptive transfer of the T-cells from the spleen of IL-37^+/+ mice following DSS treatment partly recovered the body weight, improved the disease activity index (DAI) and macroscopic damage score, and attenuated the intestinal inflammation. In addition, colon shortening, an indirect marker of inflammation, was decreased, consistent with the decreased IFN-γ level and the increased IL-10 level in the colonic tissue. Collectively, our data uncovered a subset of T-lymphocytes expressing IL-37, which represents a potent regulation of immunity and serves as the protective role in chronic IBD.