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

被引:215
|
作者
Ihara, Sozaburo [1 ,2 ]
Hirata, Yoshihiro [2 ]
Koike, Kazuhiko [2 ]
机构
[1] Asahi Life Fdn, Inst Adult Dis, Div Gastroenterol, Tokyo, Japan
[2] Univ Tokyo, Grad Sch Med, Dept Gastroenterol, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1138655, Japan
关键词
Transforming growth factor-beta; Inflammatory bowel disease; Dendritic cells; Microbiota; Adhesion molecules; SMAD7 ANTISENSE OLIGONUCLEOTIDE; MESSENGER-RNA EXPRESSION; ACTIVE CROHNS-DISEASE; T-CELLS; DENDRITIC CELLS; ULCERATIVE-COLITIS; INTRAEPITHELIAL LYMPHOCYTES; TARGETED DISRUPTION; GUT MICROBIOTA; RETINOIC-ACID;
D O I
10.1007/s00535-017-1350-1
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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.
引用
收藏
页码:777 / 787
页数:11
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