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.
Asthma is a chronic lung disease characterized by an imbalance of T-helper (Th)1/Th2 cells and their cytokine profiles. Natural killer (NK) cells constitute a considerable subset of the lymphocyte population in the lungs, and provide protection against respiratory infection by fungi, bacteria and viruses. However, the mechanism by which NK cells are involved in asthma remains to be fully elucidated. The present study analyzed the dynamic changes of NK cells and their subsets during the development of the ovalbumin (OVA)-induced allergic airway response. Lung tissues were histologically examined for cell infiltration and mucus hypersecretion. The number, activity and cytokine-secreting ability of NK cells was determined by flow cytometry. The results showed that the percentage of NK cells in the lung was decreased following OVA sensitization and challenge. However, NK cells exhibited enhanced activity and secreted more Th2 cytokines (IL-5 and IL-13) following OVA challenge. Furthermore, the proportion of CD11b− NK subsets increased with the development of asthma, and CD11b− CD27− NK cells were the primary NK subset producing Th2 cytokines. These findings suggest that, although NK cells are not the crucial type of lymphocytes involved in asthma, OVA induces NK cells to secrete Th2 cytokines that may be involved in the pathogenesis of asthma.
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