TGF-β in inflammatory bowel disease: a key regulator of immune cells, epithelium, and the intestinal microbiota

Inflammatory bowel disease (IBD) is defined as chronic intestinal inflammation, and includes ulcerative colitis and Crohn's disease. Multiple factors are involved in the pathogenesis of IBD, and the condition is characterized by aberrant mucosal immune reactions to intestinal microbes in genetically susceptible hosts. Transforming growth factor-beta (TGF-beta) is an immune-suppressive cytokine produced by many cell types and activated by integrins. Active TGF-beta binds to its receptor and regulates mucosal immune reactions through the TGF-beta signaling pathway. Dysregulated TGF-beta signaling is observed in the intestines of IBD patients. TGF-beta signal impairment in specific cell types, such as T-cells and dendritic cells, results in spontaneous colitis in mouse models. In addition, specific intestinal microbes contribute to immune homeostasis by modulating TGF-beta production. In this review, we describe the role of TGF-beta in intestinal immunity, focusing on immune cells, epithelium, and intestinal microbes. In addition, we present potential therapeutic strategies for IBD that target TGF-beta.