IL-23 and IL-2 activation of STAT5 is required for optimal IL-22 production in ILC3s during colitis
David Bauché, Barbara Joyce-Shaikh, Julie Fong, Alejandro V. Villarino, Karin S. Ku, Renu Jain, Yu‐Chi Lee, Lakshmanan Annamalai, Jennifer H. Yearley, Daniel J. Cua
Abstract
-mediated colitis and that interleukin-2 (IL-2)- and IL-23-induced STAT5 drives IL-22 production in both mouse and human colonic lamina propria ILC3s. Mechanistically, IL-23 induces a STAT3-STAT5 complex that binds IL-22 promoter DNA elements in ILC3s. Our data suggest that STAT5a/b signaling in ILC3s maintains gut epithelial integrity during pathogen-induced intestinal disease.
Topics & Concepts
STAT5Citrobacter rodentiumSTAT proteinBiologySTAT3statImmunologyInnate lymphoid cellInflammatory bowel diseaseColitisCancer researchInnate immune systemImmune systemSignal transductionCell biologyMedicineDiseaseInternal medicineIL-33, ST2, and ILC PathwaysWhipple's Disease and InterleukinsEosinophilic Esophagitis