1.
Ebbo, M, Crinier, A, Vély, F, Vivier, E. Innate lymphoid cells: major players in inflammatory diseases. Nat Rev Immunol. 2017;17:665-678. doi:
10.1038/nri.2017.86. Google Scholar |
Crossref |
Medline2.
Choy, MC, Visvanathan, K, De Cruz, P. An overview of the innate and adaptive immune system in inflammatory bowel disease. Inflamm Bowel Dis. 2017;23:2-13. doi:
10.1097/MIB.0000000000000955. Google Scholar |
Crossref |
Medline3.
Lee, SH, Kwon, JE, Cho, ML. Immunological pathogenesis of inflammatory bowel disease. Intest Res. 2018;16:26-42. doi:
10.5217/ir.2018.16.1.26. Google Scholar |
Crossref |
Medline4.
Jostins, L, Ripke, S, Weersma, RK, et al. Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease. Nature. 2012;491:119-124. doi:
10.1038/nature11582. Google Scholar |
Crossref |
Medline |
ISI5.
Liu, JZ, van Sommeren, S, Huang, H, et al. Association analyses identify 38 susceptibility loci for inflammatory bowel disease and highlight shared genetic risk across populations. Nat Genet. 2015;47:979-986. doi:
10.1038/ng.3359. Google Scholar |
Crossref |
Medline |
ISI6.
Saleh, AN, Melissa, A, Anam, K, et al. Role of ATG16L, NOD2 and IL23R in Crohn’s disease pathogenesis. World J Gastroenterol. 2012;18:412-424. doi:
10.3748/wjg.v18.i5.412. Google Scholar |
Crossref |
Medline7.
Rioux, JD, Xavier, RJ, Taylor, KD, et al. Genome-wide association study identifies new susceptibility loci for Crohn disease and implicates autophagy in disease pathogenesis. Nat Genet. 2007;39:596-604.
Google Scholar |
Crossref |
Medline |
ISI8.
Singh, SB, Davis, AS, Taylor, GA, Deretic, V. Human IRGM induces autophagy to eliminate intracellular mycobacteria. Science. 2006;313:1438-1441.
Google Scholar |
Crossref |
Medline9.
Duerr, RH, Taylor, KD, Brant, SR, et al. A genome-wide association study identifies IL23R as an inflammatory bowel disease gene. Science. 2006;314:1461-1463. doi:
10.1126/science.1135245. Google Scholar |
Crossref |
Medline |
ISI10.
Fisher, S, Tremelling, M, Anderson, CA, et al. Genetic determinants of ulcerative colitis include the ECM1 locus and five loci implicated in Crohn’s disease. Nat Genet. 2008;40:710-712. doi:
10.1038/ng.145. Google Scholar |
Crossref |
Medline |
ISI11.
Huttenhower, C, Kostic, AD, Xavier, RJ. Inflammatory bowel disease as a model for translating the microbiome. Immunity. 2014;40:843-854. doi:
10.1016/j.immuni.2014.05.013. Google Scholar |
Crossref |
Medline12.
Bernstein, CN, Blanchard, JF, Rawsthorne, P, Yu, N. The prevalence of extraintestinal diseases in inflammatory bowel disease: a population-based study. Am J Gastroenterol. 2001;96:1116-1122.
Google Scholar |
Crossref |
Medline |
ISI13.
Levine, JS, Burakoff, R. Extra-intestinal manifestations of inflammatory bowel disease. Gastroenterol Hepatol (NY). 2011;7:235-241.
Google Scholar14.
Agouridis, AP, Elisaf, M, Milionis, HJ. An overview of lipid abnormalities in patients with inflammatory bowel disease. Ann Gastroenterol. 2011;24:181-187.
Google Scholar |
Medline15.
Akerlund, JE, Reihnér, E, Angelin, B, et al. Hepatic metabolism of cholesterol in Crohn’s disease. Effect of partial resection of ileum. Gastroenterology. 1991;100:1046-1053. doi:
10.1016/0016-5085(91)90281-o. Google Scholar |
Crossref |
Medline16.
Gillen, CD, Walmsley, RS, Prior, P, Andrews, HA, Allan, RN. Ulcerative colitis and Crohn’s disease: a comparison of the colorectal cancer risk in extensive colitis. Gut. 1994;35:1590-1592.
Google Scholar |
Crossref |
Medline |
ISI17.
Giovannucci, E, Ascherio, A, Rimm, EB, Colditz, GA, Stampfer, MJ, Willett, WC. Physical activity, obesity, and risk for colon cancer and adenoma in men. Ann Intern Med. 1995;122:327-334.
Google Scholar |
Crossref |
Medline |
ISI18.
Hass, DJ, Brensinger, CM, Lewis, JD, Lichtenstein, GR. The impact of increased body mass index on the clinical course of Crohn’s disease. Clin Gastroenterol Hepatol. 2006;4:482-488.
Google Scholar |
Crossref |
Medline |
ISI19.
Darfeuille-Michaud, A, Neut, C, Barnich, N, et al. Presence of adherent Escherichia coli strains in ileal mucosa of patients with Crohn’s disease. Gastroenterology. 1998;115:1405-1413. doi:
10.1016/s0016-5085(98)70019-8. Google Scholar |
Crossref |
Medline |
ISI20.
Hugot, JP, Chamaillard, M, Zaouli, H, Lesage, S, Cézard, JP, Belaiche, J. Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn’s disease. Nature. 2001;411:599-603.
Google Scholar |
Crossref |
Medline |
ISI21.
Hart, AL, Al-Hassi, HO, Rigby, RJ, et al. Characteristics of intestinal dendritic cells in inflammatory bowel diseases. Gastroenterology. 2005;129:50-65.
Google Scholar |
Crossref |
Medline |
ISI22.
Wagner, J, Sim, WH, Ellis, JA, et al. Interaction of Crohn’s disease susceptibility gene in an Australian paediatric cohort. PLoS ONE. 2010;5:e1537. doi:
10.1371/journal.pone.0015376. Google Scholar |
Crossref23.
Lesage, S, Zouali, H, Cézard, JP, et al. CARD15/NOD2 mutational analysis and genotype-phenotype correlation in 612 patients with inflammatory bowel disease. Am J Hum Genet. 2002;70:845-857. doi:
10.1086/339432. Google Scholar |
Crossref |
Medline24.
Xia, B, Crusius, JB, Wu, J, Zwiers, A, van Bodegraven, AA, Peña, AS. CTLA4 gene polymorphisms in Dutch and Chinese patients with inflammatory bowel disease. Scand J Gastroenterol. 2002;37:1296-1300.
Google Scholar |
Crossref |
Medline25.
Brand, S, Staudinger, T, Schnitzler, F, Pfennig, S, et al. The role of Toll-like receptor 4 Asp299Gly and Thr399Ile polymorphisms and CARD15/NOD2 mutations in the susceptibility and phenotype of Crohn’s disease. Inflamm Bowel Dis. 2005;11:645-652.
Google Scholar |
Crossref |
Medline26.
Cummings, JR, Ahmad, T, Geremia, A, et al. Contribution of the novel inflammatory bowel disease gene IL23R to disease susceptibility and phenotype. Inflamm Bowel Dis. 2007;13:1063-1068.
Google Scholar |
Crossref |
Medline27.
Cho, JH. Inflammatory bowel disease: genetic and epidemiologic considerations. World J Gastroenterol. 2008;14:338-347.
Google Scholar |
Crossref |
Medline28.
Read, S, Malmström, V, Powrie, F. Cytotoxic T lymphocyte associated antigen 4 plays an essential role in the function of CD25 (+) CD4 (+) regulatory cells that control intestinal inflammation. J Exp Med. 2000;192:295-302.
Google Scholar |
Crossref |
Medline |
ISI29.
Brest, P, Lapaquette, P, Souidi, M, et al. A synonymous variant in IRGM alters a binding site for miR-196 and causes deregulation of IRGM-dependent xenophagy in Crohn’s disease. Nat Genet. 2011;43:242-245.
Google Scholar |
Crossref |
Medline |
ISI30.
Hampe, J, Franke, A, Rosenstiel, P, et al. A genome-wide association scan of nonsynonymous SNPs identifies a susceptibility variant for Crohn disease in ATG16L1. Nat Genet. 2007;39:207-211.
Google Scholar |
Crossref |
Medline |
ISI31.
Cadwell, K, Liu, JY, Brown, SL, et al. A key role for autophagy and the autophagy gene Atg16l1 in mouse and human intestinal Paneth cells. Nature. 2008;456:259-263.
Google Scholar |
Crossref |
Medline |
ISI32.
Kuballa, P, Huett, A, Rioux, JD, Daly, MJ, Xavier, RJ. Impaired autophagy of an intracellular pathogen induced by a Crohn’s disease associated ATG16L1 variant. PLoS ONE. 2008;3:e3391. doi:
10.1371/journal.pone.0003391. Google Scholar |
Crossref |
Medline33.
Glas, J, Seiderer, J, Bues, S, et al. IRGM variants and susceptibility to inflammatory bowel disease in the German population. PLoS ONE. 2013;8:e54338. doi:
10.1371/journal.pone.0054338. Google Scholar |
Crossref34.
Glas, J, Wagner, J, Seiderer, J, et al. PTPN2 gene variants are associated with susceptibility to both Crohn’s disease and ulcerative colitis supporting a common genetic disease background. PLoS ONE. 2012;7:e33682. doi:
10.1371/journal.pone.0033682. Google Scholar |
Crossref35.
Scharl, M, Mwinyi, J, Fischbeck, A, et al. Crohn’s disease-associated polymorphism within the PTPN2 gene affects muramyl-dipeptide-induced cytokine secretion and autophagy. Inflamm Bowel Dis. 2012;18:900-912.
Google Scholar |
Crossref |
Medline36.
Barrett, JC, Hansoul, S, Nicolae, DL, et al. Genome-wide association defines more than 30 distinct susceptibility loci for Crohn’s disease. Nat Genet. 2008;40:955-962.
Google Scholar |
Crossref |
Medline |
ISI37.
Henckaerts, L, Cleynen, I, Brinar, M, et al. Genetic variation in the autophagy gene ULK1 and risk of Crohn’s disease. Inflamm Bowel Dis. 2011;17:1392-1397.
Google Scholar |
Crossref |
Medline38.
Franchimont, D, Vermeire, S, El Housni, H, et al. Deficient host-bacteria interactions in inflammatory bowel disease? The toll-like receptor (TLR)-4 Asp299gly polymorphism is associated with Crohn’s disease and ulcerative colitis. Gut. 2004;53:987-992.
Google Scholar |
Crossref |
Medline |
ISI39.
Michail, S, Bultron, G, DePaolo, RW. Genetic variants associated with Crohn’s disease. Appl Clin Genet. 2013;6:25-32.
Google Scholar |
Crossref |
Medline40.
Ken, YH, Heriberto, FH, Jianzhong, H, et al. Functional variants in the LRRK2 gene confer shared effect on risk for Crohn’s disease and Parkinson’s disease. Sci Transl. Med. 2018;10:1-31.
Google Scholar41.
Franke, A, Balschun, T, Sina, C, Ellinghaus, D, et al. Genome-wide association study for ulcerative colitis identifies risk loci at 7q22 and 22q13 (IL17REL). Nat Genet. 2010;42:292-294. doi:
10.1038/ng.553. Google Scholar |
Crossref |
Medline42.
Ogura, Y, Bonen, DK, Inohara, N, et al. A frameshift mutation in NOD2 associated with susceptibility to Crohn’s disease. Nature. 2001;411:603-606.
Google Scholar |
Crossref |
Medline |
ISI43.
Strober, W, Watanabe, T. NOD2, an intracellular innate immune sensor involved in host defense and Crohn’s disease. Mucosal Immunol. 2011;4:484-495.
Google Scholar |
Crossref |
Medline44.
Kullberg, BJ, Ferwerda, G, de Jong, DJ, et al. Crohn’s disease patients homozygous for the 3020insC NOD2 mutation have a defective NOD2/TLR4 cross-tolerance to intestinal stimuli. Immunology. 2008;123:600-605.
Google Scholar |
Crossref |
Medline45.
Lapaquette, P, Bringer, MA, Darfeuille-Michaud, A. Defects in autophagy favour adherent-invasive Escherichia coli persistence within macrophages leading to increased pro-inflammatory response. Cell Microbiol. 2012;14:791-807. doi:
10.1111/j.1462-5822.2012.01768.x. Google Scholar |
Crossref |
Medline
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