作者: Maria T. Abreu , Miles P. Sparrow
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摘要: The idiopathic inflammatory bowel diseases (IBDs), broadly classified as either Crohn's disease (CD) or ulcerative colitis (UC), are caused by a dysregulated mucosal immune response to luminal antigen, possibly bacterium, in genetically predisposed host. A rapid expansion of knowledge recent years has greatly increased our understanding the pathophysiology these disorders. For example, relatively discovery NOD2 gene, protein involved bacterial sensing, provided further evidence complex interplay between hosts and microbes disease. Significant advances have also occurred with role Toll-like receptors dendritic cells development gut inflammation, proinflammatory cytokines potentiation inflammation. This article presents an update on key developments emphasizes translational aspects research that directly related patient care.