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• W47367076 abstract "During the last few years significant advances have been achieved in the understanding of the pathogenesis of inflammatory bowel disease (IBD). A genetic susceptibility to Crohn's disease has been proven by identification of variations as risk factor NOD2/CARD15. Functional data on NOD2/CARD15 and NF-kappaB activation indicate that an inflammatory reaction of the intestinal mucosa, as an immediate response of the innate immune system, may be necessary for the maintenance of gut homeostasis. Crohn's disease is now also discussed as an impaired and inadequate immune reaction and no longer only as a hyper-responsiveness of the mucosal immune system. Data on NOD2/CARD15 expression suggest that macrophages and epithelial cells could be the locus of the primary pathophysiological defect and that T-cell activation might just be a secondary effect inducing chronification of the inflammation, perhaps as backup mechanism to insufficient innate immunity. In addition to NOD2/CARD15 there are more innate pathways by which commensal and pathogenic bacteria can directly be hindered to invade the human body (such as interaction with Toll like receptors, TLRs and defensins). The germ-concept and the genetic concept of IBD pathophysiology are converging. However, more time is needed until these important insights in IBD pathogenesis will make their way into routine diagnostic procedures and treatment of patients with IBD." @default.
• W47367076 created "2016-06-24" @default.
• W47367076 creator A5050651546 @default.
• W47367076 creator A5058012401 @default.
• W47367076 date "2009-09-19" @default.
• W47367076 modified "2023-09-24" @default.
• W47367076 title "New insights into the pathogenesis of Crohn’s disease: are they relevant for therapeutic options?" @default.
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• W47367076 doi "https://doi.org/10.4414/smw.2009.12520" @default.
• W47367076 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19838869" @default.
• W47367076 hasPublicationYear "2009" @default.
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