Immunology of inflammatory bowel disease

Recent studies in the immunology of inflammatory bowel disease (IBD) have focused on several areas: definition of pathogenic mechanisms, discovery of etiologic agents, development or refinement of new diagnostic tests, and identification of targets for immunologically based therapy. The repertoire of T lymphocytes is different in the gut compared with the peripheral blood in both healthy control subjects and patients with IBD. There is as yet, however, no evidence that activation of these cells is due to a single antigen or superantigen, and it is not clear whether this activation is specific for IBD. Bacterial peptidoglycan-polysaccharide complexes have been found within the gut wall in patients with Crohn's disease, and these antigens produce a higher T-lymphocyte proliferative response in this group compared with control subjects. B-cell function is also altered in IBD, in the classes and subclasses of immunoglobulin secretion. Lower HLA class II antigen expression by monocytes is also seen in IBD, and preliminary studies suggest that this correlates with poor outcome. Further characterization of the antineutrophil cytoplasmic antibody has been done within different populations, but the exact target of this antibody within the neutrophil remains unknown. Another autoantibody targeting colonic epithelial cells in patients with ulcerative colitis has also been shown to bind to epitopes of epithelial cells in the biliary tract, ciliary cells in the eye, and chondrocytes in the joint space. Adhesion molecules continue to be studied, but no specific alterations have been found in IBD compared with bowel inflammation from other causes.