Ulcerative colitis (UC) and Crohn's disease (CD), collectively referred to as inflammatory bowel disease (IBD), present with differing histologic and cytokine profiles. While the precise mechanisms underlying the development of IBD are not known, sufficient data have been collected to suggest that it results from a complex interplay of genetic, environmental, and immunologic factors. Animal models of colitis, along with a more detailed understanding of the immune response in the normal bowel, have led to unifying hypotheses regarding the pathogenesis. An inappropriate mucosal immune response to normal intestinal constituents is a key feature, leading to an imbalance in local pro- and anti-inflammatory cytokines. Neutrophil and monocyte influx occurs with subsequent secretion of oxygen radicals and enzymes, leading to tissue damage. Therapy of IBD has improved and expanded as the understanding of disease mechanisms has evolved. Pharmacologic agents such as aminosalicylates, azathioprine/6-mercaptopurine, or steroids are the mainstays of therapy. Newer agents including monoclonal antibodies targeted to specific proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha), have emerged and provide great clinical benefit, but unknown long-term toxicity and immunogenicity may limit their use.