Examination of T-cell function in both animal models and patients with inflammatory bowel disease (IBD) has consistently demonstrated the importance of interleukin-12-driven T-helper 1 CD4 plus; T-cell responses, with resultant secretion of interferon-gamma;, interleukin- 1 beta;, and tumor necrosis factor. Demonstration of this central regulatory pathway in the immunopathogenesis of IBD will allow novel, selective therapeutic approaches to be developed and appropriately evaluated in both animal models and patients with IBD. Studies of autoantibodies in IBD continue to demonstrate the possible importance of antineutrophil cytoplasmic antibodies in delineating subsets of patients with chronic IBD. Delineation of histones as well as nonhistone nuclear antigens as possible targets for perinuclear antineutrophil cytoplasmic antibodies provides an exciting new area for future research. The examination of specific adhesion molecules on endothelial cells has revealed that they may play important roles in both extraintestinal manifestations of IBD as well as the initiation and perpetuation of mucosal inflammatory processes. Nitric oxide and reactive oxygen metabolites are important mediators as well as markers of mucosal inflammation and injury in IBD. Inducible nitric oxide synthease may play an important role in mucosal healing and recovery from intestinal injury.
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