自噬在炎症性肠病中作用机制的研究进展

Research updates: the mechanism of autophagy in inflammatory bowel disease

炎症性肠病(IBD)是一种起病缓慢、病情轻重不一的、易反复发作的非特异性肠道炎症性疾病,病因和发病机制尚未完全明确,当前认为是由包括环境、遗传、感染和免疫等多因素相互作用所致。自噬可以通过参与病原体清除、影响免疫功能、调节炎症信号或抑制炎性体(inflammasome)等多种途径参与IBD的免疫应答。研究发现自噬相关蛋白16样分子1(ATG16L1)、免疫相关鸟苷三磷酸酶M(IRGM)、核苷酸结合寡聚结构域蛋白2(NOD2)是与IBD有关的高度易感基因,基因的缺失和突变影响IBD的发生发展。我们总结了自噬及其相关基因在IBD中调节细胞因子分泌、调控免疫应答等作用机制。

Inflammatory bowel disease(IBD) is a non-specific intestinal inflammatory disease with slow onset, varying severity and recurrence. Even though the causes of IBD are still unknown, studies have indicated that the pathogenesis of IBD is associated with multiple factors, including environment, genetics, infection and immunity. Autophagy is involved in regulating the immune response of IBD through a variety of ways such as pathogen removal, immune function, regulation of inflammatory signals, or inhibition of inflammasomes. Recent studies suggested that autophagy-related genes including ATG16L1, IRGM, and NOD2 are highly susceptible genes related to IBD, and gene deletion and mutation affect the occurrence and development of IBD. Hereby, we review the mechanism of autophagy and its related genes regulating the cytokines secretion and adjusting the immune response in IBD.