TNF 启动子低甲基化与 IBD 黏膜炎症和抗 TNF 反应有关

Daniel S. Levic, Donna Niedzwiecki, Apoorva Kandakatla, Norah S. Karlovich, Arjun Juneja, Jieun Park, Christina Stolarchuk, Shanté Adams, Jason R. Willer, Matthew R. Schaner, Grace Lian, Caroline Beasley, Lindsay Marjoram, Ann D. Flynn, John F. Valentine, Jane E. Onken, Shehzad Z. Sheikh, Erica E. Davis, Kimberley J. Evason, Katherine S. Garman, Michel Bagnat
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摘要

背景和目的 炎症性肠病(IBD)是受环境因素严重影响的慢性炎症性疾病。DNA 甲基化是一种表观遗传调控形式,它将环境刺激与基因表达变化和炎症联系在一起。在此,我们研究了 IBD 患者(包括抗肿瘤坏死因子应答者和非应答者)有炎症和无炎症粘膜之间 TNF 启动子 DNA 甲基化的差异。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
TNF promoter hypomethylation is associated with mucosal inflammation in IBD and anti-TNF response
Background and aims Inflammatory Bowel Diseases (IBD) are chronic inflammatory conditions influenced heavily by environmental factors. DNA methylation is a form of epigenetic regulation linking environmental stimuli to gene expression changes and inflammation. Here, we investigated how DNA methylation of the TNF promoter differs between inflamed and uninflamed mucosa of IBD patients, including anti-TNF responders and non-responders.
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