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It has led to the discovery of mutations in <jats:italic>NOD2<\/jats:italic> associated with ileal CD and numerous other genes have been found to be associated with IBD susceptibility.<\/jats:p><jats:p><jats:bold>Methods\u2002<\/jats:bold> A review of the literature on the genetic background of IBD was performed.<\/jats:p><jats:p><jats:bold>Results\u2002<\/jats:bold> It is only partially understood how mutations in <jats:italic>NOD2<\/jats:italic> lead to CD. Mouse models, <jats:italic>in vitro<\/jats:italic> data and studies in humans offer conflicting data as regards whether there is a loss or gain of function of NOD2 in CD. Several additional genes have been identified of which only a few are currently being recognized as potential disease causing or disease modifying genes. Promising candidate genes include <jats:italic>TLR4, MDR1, NOD1 (CARD4), DLG5<\/jats:italic> as well as the IBD5 locus including <jats:italic>SLC22A4\/5<\/jats:italic>.<\/jats:p><jats:p><jats:bold>Conclusions\u2002<\/jats:bold> Although genetic research has not yet led to a better prediction of the disease course or patient selection for medical therapy, remarkable progress has been made in the understanding of the pathogenesis of IBD. For future genetic research, accurate phenotyping of patients is very important and large population\u2010based cohorts are needed. Eventually, genetic research may be able to classify different disease phenotypes on a more detailed molecular basis and may provide important contributions in the development of new therapeutic approaches.<\/jats:p>","DOI":"10.1111\/j.1365-2036.2007.03476.x","type":"journal-article","created":{"date-parts":[[2010,7,23]],"date-time":"2010-07-23T14:00:50Z","timestamp":1279893650000},"page":"57-65","source":"Crossref","is-referenced-by-count":21,"title":["Review article: inflammatory bowel disease and genetics"],"prefix":"10.1111","volume":"26","author":[{"given":"R. K.","family":"WEERSMA","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H. M.","family":"VAN DULLEMEN","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G.","family":"VAN DER STEEGE","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"I. 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