Clermont Université, Université d'Auvergne, Clermont-Ferrand, France.
J Mol Med (Berl). 2012 Sep;90(9):987-96. doi: 10.1007/s00109-012-0934-8. Epub 2012 Jul 14.
Crohn's disease is a complex multifactor diseases that occur in individuals with genetic predisposition in whom environmental and microbial triggers cause a deleterious chronic immune response. Susceptibility to Crohn's disease is influenced by common variants at many loci. Genetic studies have emphasized the role of host susceptibility in inflammatory bowel disease onset with the identification of about 100 risk loci, most of which encode proteins involved in immunity, host defense against microbes, and gut homeostasis. In this review, we focus on susceptibility genes related to autophagy in the etiology of Crohn's disease (CD) and their complex interplay with the gut microbiota, as illustrated by the relationship between immunity-related GTPase family M alleles, microRNA, and xenophagy in CD predisposition.
克罗恩病是一种复杂的多因素疾病，发生在具有遗传易感性的个体中，环境和微生物触发因素导致有害的慢性免疫反应。克罗恩病的易感性受许多基因座常见变异的影响。遗传研究强调了宿主易感性在炎症性肠病发病中的作用，确定了约 100 个风险基因座，其中大多数编码参与免疫、宿主防御微生物和肠道内稳态的蛋白质。在这篇综述中，我们重点关注与克罗恩病发病机制中的自噬相关的易感基因及其与肠道微生物群的复杂相互作用，如图所示，免疫相关 GTPase 家族 M 等位基因、微小 RNA 和 CD 易感性中的异噬之间的关系。
