Epigenetic regulation of T helper cells and intestinal pathogenicity

被引:20
作者
Hagihara, Yuya [1 ]
Yoshimatsu, Yusuke [1 ]
Mikami, Yohei [1 ]
Takada, Yoshiaki [1 ]
Mizuno, Shinta [1 ]
Kanai, Takanori [1 ,2 ]
机构
[1] Keio Univ, Sch Med, Dept Internal Med, Div Gastroenterol & Hepatol,Shinjuku Ku, Tokyo 1608582, Japan
[2] Japan Agcy Med Res & Dev, CREST, AMED, Tokyo 1000004, Japan
基金
日本学术振兴会;
关键词
CD4 T cell; Colitis; Mucosal immunology; Inflammatory bowel disease; Epigenetic regulation; ROR-GAMMA-T; RECOMBINANT HUMAN INTERLEUKIN-10; HISTONE DEACETYLASE INHIBITORS; INFLAMMATORY-BOWEL-DISEASE; LONG NONCODING RNA; TRANSCRIPTION FACTOR; ULCERATIVE-COLITIS; TH17; CELLS; TGF-BETA; INTERFERON-GAMMA;
D O I
10.1007/s00281-019-00732-9
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Inflammatory bowel diseases (IBDs) are characterized by relapsing and remitting chronic intestinal inflammation. Previous studies have demonstrated the contributions of genetic background, environmental factors (food, microbiota, use of antibiotics), and host immunity in the development of IBDs. More than 200 genes have been shown to influence IBD susceptibility, most of which are involved in immunity. The vertebrate immune system comprises a complex network of innate and adaptive immune cells that protect the host from infection and cancer. Dysregulation of the mutualistic relationship between the immune system and the gut environment results in IBD. Considering the fundamental role of epigenetic regulation in immune cells, epigenetic mechanisms, particularly in T helper (Th) cells, may play a major role in the complex regulation of mucosal immunity. Epigenetic regulation and dysregulation of Th cells are involved in the maintenance of intestinal homeostasis and its breakdown in IBD.
引用
收藏
页码:379 / 399
页数:21
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