摘要
溃疡性结肠炎(ulcerative colitis,UC)是一种由多种内外因素造成的以结肠黏液屏障损伤为病理基础的炎症性肠病,其中局部免疫系统和肠道菌群紊乱是导致肠道黏液屏障损伤的重要因素。黏蛋白组成了肠道黏液层的主要部分,可由杯状细胞产生,其翻译后修饰模式为O-糖基化。黏蛋白型O-糖基化不仅能够保证黏液层的完整性,同时还可通过调控免疫系统及肠道菌群参与UC的发生、发展。该文就黏蛋白型O-糖基化在UC发病机制中的主要作用进行综述,旨在为防治UC提供新思路。
Ulcerative colitis(UC)is an inflammatory bowel disease based on the pathological damage of the colon mucus barrier due to a variety of internal and external factors.The disorders of local immune system and intestinal flora are important factors leading to the damage of intestinal mucus barrier.Mucins,a major component of the intestinal mucus layer,are produced by goblet cells and may be post-translational modified by O-glycosylation.Mucin-type O-glycosylation not only ensures the integrity of the mucus layer,but also participates in the occurrence and development of UC by regulating the immune system and intestinal flora.This review summarizes the main mechanism of mucin-type O-glycosylation in the pathogenesis of UC,aiming to provide new ideas for prevention and treatment of UC.
作者
杨新棵
周永学
杨铭杰
闫曙光
YANG Xinke;ZHOU Yongxue;YANG Mingjie;YAN Shuguang(School of Basic Medicine,Shaanxi University of Chinese Medicine,Xianyang 712046,China)
出处
《现代免疫学》
2025年第3期328-333,共6页
Current Immunology
基金
国家自然科学基金(81873233
82374328)。
作者简介
杨新棵(1998-),男,硕士生,主要从事胃肠病研究;通信作者:闫曙光(E-mail:ysg2002.student@sina.com)。
