Epithelial autophagy controls chronic colitis by reducing TNF-induced apoptosis.
Epithelial autophagy controls chronic colitis by reducing TNF-induced apoptosis.
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DOI：
10.1080/15548627.2018.1450021
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发表时间：
2018
期刊：
影响因子：
13.3
通讯作者：
Maloy KJ
中科院分区：
文献类型：
--
作者：
Pott J;Maloy KJ
全基因组关联研究（GWAS）将ATG 16 L1多态性与炎症性肠病（IBD）易感性联系起来，促使粘膜免疫学家研究肠道中不同细胞类型中巨自噬/自噬的功能作用。在这里，我们提出了一项最近的研究，解决了两个关键问题：在慢性结肠炎期间，哪种细胞类型的自噬缺陷最有害，以及自噬在这些细胞中的功能作用是什么？我们报告说，肠上皮细胞（IEC）的自噬作用，以限制肠道炎症，保护他们从TNF诱导的凋亡，我们讨论了IBD治疗的潜在影响。
Genome-wide association studies (GWAS) linking polymorphisms in ATG16L1 with susceptibility to inflammatory bowel disease (IBD) have prompted mucosal immunologists to investigate the functional roles of macroautophagy/autophagy in different cell types in the gut. Here we present a recent study that addressed 2 key questions: in which cell type is autophagy deficiency most detrimental during chronic colitis and what is the functional role of autophagy in those cells? We report that autophagy in intestinal epithelial cells (IECs) acts to limit intestinal inflammation by protecting them from TNF-induced apoptosis and we discuss the potential implications for IBD treatment.