摘要
炎症性肠病(inflammatory bowel disease,IBD)的表观遗传学研究发现DNA甲基化是发生在基因组Cp G二核苷酸的胞嘧啶上的变化,溃疡性结肠炎(ulcerative colitis,UC)有16%的遗传可能性;IBD的免疫学研究发现本病存在由CD4+Th1、Th2、Th17、Treg淋巴细胞介导的免疫反应;肠道菌群失调是IBD的继发性改变,但其在黏膜免疫反应及炎症的持续及放大效应中发挥重要作用;肠黏膜在抵御肠道菌群的过程中发挥重要作用,回肠克罗恩病(Crohn’s disease,CD)与防御素表达减少或功能缺陷有关,且肠黏膜紧密连接(tight junction,TJ)的复杂性受损。
The epigenetics of inflammatory bowel disease （IBD） has found that DNA methylation is an epigenetic change occurring at cytosines in CpG dinucleotides and ulcerative colitis （UC） has 16% of heritability. The immunological research has also found that IBD is characterized by the presence of dysregulated immune responses governed by the activi- ties of CD4 ＋ Thl, Th2, Th17 and Treg lymphocytes. The imbalance of intestinal flora is the secondary change of IBD, but it plays an important role in mucosal immune response and persistent inflammation and amplification effect. Intestinal mu- cosa plays an important role in the process of fighting against intestinal flora. Ileal Crohn＇ s disease （CD） is associated with reduced expression of defense or functional defects, and the complexity of intestinal mucosa tight junction （TJ） is damaged.
出处
《胃肠病学和肝病学杂志》
CAS
2016年第7期733-735,共3页
Chinese Journal of Gastroenterology and Hepatology
基金
国家自然科学基金(81173392)
关键词
炎症性肠病
表观遗传
免疫反应
肠道菌群
防御素
紧密连接
Inflammatory bowel disease
Epigenetics
Immune responses
Intestinal flora
Defensins
Tight junction
