| Literature DB >> 28534191 |
Sozaburo Ihara1,2, Yoshihiro Hirata3, Kazuhiko Koike2.
Abstract
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-β (TGF-β) is an immune-suppressive cytokine produced by many cell types and activated by integrins. Active TGF-β binds to its receptor and regulates mucosal immune reactions through the TGF-β signaling pathway. Dysregulated TGF-β signaling is observed in the intestines of IBD patients. TGF-β 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-β production. In this review, we describe the role of TGF-β in intestinal immunity, focusing on immune cells, epithelium, and intestinal microbes. In addition, we present potential therapeutic strategies for IBD that target TGF-β.Entities:
Keywords: Adhesion molecules; Dendritic cells; Inflammatory bowel disease; Microbiota; Transforming growth factor-β
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Year: 2017 PMID： 28534191 DOI： 10.1007/s00535-017-1350-1
Source DB: PubMed Journal: J Gastroenterol ISSN： 0944-1174 Impact factor: 7.527