Linking Immunity, Epigenetics, and Cancer in Inflammatory Bowel Disease

被引：38
作者：
Daebritz, Jan [1 ,2 ,3 ]
Menheniott, Trevelyan R. [1 ,2 ]
机构：
[1] Royal Childrens Hosp, Murdoch Childrens Res Inst, Parkville, Vic 3052, Australia
[2] Univ Melbourne, Melbourne Med Sch, Dept Paediat, Parkville, Vic 3052, Australia
[3] Univ Childrens Hosp Munster, Dept Pediat Rheumatol & Immunol, Munster, Germany
来源：
INFLAMMATORY BOWEL DISEASES | 2014年 / 20卷 / 09期
基金：
英国医学研究理事会;
关键词：
DNA methylation; histone modification; micro RNAs; microbiota; colitis-associated cancer; Crohn's disease; ulcerative colitis; cytokines; host defense; gene-environment interactions; innate immunity; adaptive immunity; animal models; DE-NOVO METHYLATION; DNA METHYLTRANSFERASES DNMT3A; CHROMATIN REMODELING COMPLEX; INTESTINAL EPITHELIAL-CELLS; CPG ISLAND METHYLATION; EMBRYONIC STEM-CELLS; ULCERATIVE-COLITIS; HISTONE-MODIFICATION; CROHNS-DISEASE; PROMOTER HYPERMETHYLATION;
D O I：
10.1097/MIB.0000000000000063
中图分类号：
R57 [消化系及腹部疾病];
学科分类号：
摘要：
Most of what is known about the pathogenesis of inflammatory bowel disease (IBD) pertains to complex interplay between host genetics, immunity, and environmental factors. Epigenetic modifications play pivotal roles in intestinal immunity and mucosal homeostasis as well as mediating gene-environment interactions. In this article, we provide a historical account of epigenetic research either directly related or pertinent to the pathogenesis and management of IBD. We further collate emerging evidence supporting roles for epigenetic mechanisms in relevant aspects of IBD biology, including deregulated immunity, host-pathogen recognition and mucosal integrity. Finally, we highlight key epigenetic mechanisms that link chronic inflammation to specific IBD comorbidities, including colitis-associated cancer and discuss their potential utility as novel biomarkers or pharmacologic targets in IBD therapy.
引用
收藏
页码：1638 / 1654
页数：17
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