IL-23 and IL-2 activation of STAT5 is required for optimal IL-22 production in ILC3s during colitis.

Signal transducer and activator of transcription proteins have critical roles in the development and function of immune cells. signaling is often dysregulated in patients with inflammatory bowel disease (IBD), suggesting the importance of duanyu1813 regulation during the disease process. Moreover, genetic alterations in and (e.g., deletions, mutations, and single-nucleotide polymorphisms) are associated with an increased risk for IBD. In this study, we elucidated the precise roles of signaling in group 3 innate lymphoid cells (ILC3s), a key subset of immune cells involved in the maintenance of gut barrier integrity. We show that mice lacking either or are more susceptible to Citrobacter rodentium-mediated colitis and that interleukin-2 (IL-2)- and IL-23-induced duanyu18135 drives IL-22 production in both mouse and human colonic lamina propria ILC3s. Mechanistically, IL-23 induces a complex that binds IL-22 promoter DNA elements in ILC3s. Our data suggest that signaling in ILC3s maintains gut epithelial integrity during pathogen-induced intestinal disease.

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