Autophagy and Crohn's Disease

被引:78
|
作者
Hang Thi Thu Nguyen [1 ,2 ]
Lapaquette, Pierre [4 ]
Bringer, Marie-Agnes [1 ,2 ]
Darfeuille-Michaud, Arlette [1 ,2 ,3 ]
机构
[1] Univ dAuvergne, INSERM, UMR 1071, Clermont Ferrand, France
[2] INRA, USC 2018, Clermont Ferrand, France
[3] Ctr Hosp Univ, Clermont Ferrand, France
[4] Inst Pasteur, INSERM, U993, F-75724 Paris, France
关键词
Autophagy; Crohn's disease; Adherent-invasive Escherichia coli; Nucleotide Oligomerization Domain 2; ATG16L1; IRGM; INFLAMMATORY-BOWEL-DISEASE; GENOME-WIDE ASSOCIATION; SUSCEPTIBILITY LOCI; IMPAIRED AUTOPHAGY; GENE ATG16L1; IRGM; COLI; NOD2; LRG-47; MOUSE;
D O I
10.1159/000345129
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Advances in genetics have shed light on the molecular basis of Crohn's disease (CD) predisposition and pathogenesis, via linkage disequilibrium analysis to genome-wide association studies. The discovery of genetic variants of NOD2, an intracellular pathogen molecular sensor, as risk factors for CD has paved the way for further research on innate immunity in this disease. Remarkably, polymorphisms in autophagy genes, such as ATG16L1 and IRGM, have been identified, allowing the pivotal role of autophagy in innate immunity to be uncovered. In this review, we summarize recent studies on the CD-associated NOD2, ATG16L1 and IRGM risk variants and their contribution to the autophagy functions that have most influenced our understanding of CD pathophysiology. Copyright (c) 2013 S. Karger AG, Basel
引用
收藏
页码:434 / 443
页数:10
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