自噬异常在炎症性肠病发病机制中的作用

摘要

炎症性肠病（ IBD）是一种慢性、非特异性肠道炎性疾病，其发病机制与环境、遗传以及免疫等多种因素相关。自噬在细胞稳态和机体免疫中发挥重要作用，自噬异常可能参与IBD的发病。全基因组关联分析（ GWAS）研究证实，ATG16L1、IRGM、NOD2等自噬相关基因与IBD密切相关。本文就自噬异常在IBD发病机制中的作用作一综述。%Inflammatory bowel disease( IBD)is a chronic and nonspecific intestinal inflammatory disease caused by multiple factors such as environment,genetic susceptibility and immune disturbance. Autophagy plays an important role in cellular homeostasis and immune. Autophagy abnormalities may be involved in the pathogenesis of IBD. Genome-wide association studies(GWAS)have provided compelling evidence that autophagy related genes,including ATG16L1,IRGM and NOD2,are significantly associated with IBD. This article reviewed the abnormal autophagy in pathogenesis of IBD.