Inflammatory Bowel Disease

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Abstract
The idiopathic inflammatory bowel diseases comprise two types of chronic intestinal disorders: Crohn's disease and ulcerative colitis. Accumulating evidence suggests that inflammatory bowel disease results from an inappropriate inflammatory response to intestinal microbes in a genetically susceptible host. Genetic studies highlight the importance of host–microbe interactions in the pathogenesis of these diseases.1-13 Prominent among these genetic findings are genomic regions containing nucleotide oligomerization domain 2 (NOD2),14 autophagy genes,4,7,8,10 and components of the interleukin-23–type 17 helper T-cell (Th17) pathway.2 The NOD2 protein is an intracellular sensor of bacterial peptidoglycan, and autophagy enables cells to regulate and degrade diverse intracellular components, including pathogens. 15 The autophagy gene, ATG16L1, has been associated with Crohn's disease but not, thus far, with ulcerative colitis. The interleukin-23–Th17 pathway mediates microbial defense and intestinal inflammation.16,17 Multiple genes regulating this pathway have been associated with both Crohn's disease and ulcerative colitis. This review summarizes recent progress in studies of intestinal immunity and genetics in inflammatory bowel disease.