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The etiologies of Crohn's disease and ulcerative colitis, the 2 major forms of inflammatory bowel disease in humans, remain unknown, but experimental studies suggest that inflammatory bowel disease results from interaction between environmental and genetic factors, which promotes an exaggerated and inappropriately controlled inflammatory response that is directed against normal components of the gut flora. There is also evidence that tissue damage is due to a dynamic interplay between immune and nonimmune cells, and recruitment of lymphocytes from the blood stream to the gut wall is crucial for amplifying and sustaining the ongoing mucosal inflammation. These advances have led to the development of several compounds blocking gut homing of effector lymphocytes, which have recently been used or are now ready to move into clinical practice. This article summarizes the recent data on the use of integrin-targeting and adhesion molecule–targeting therapeutics to attenuate the detrimental inflammatory response in inflammatory bowel disease.