Characterization of lymphocyte populations in the intestinal mucosa in inflammatory bowel disease (IBD) has demonstrated expansion of α, β T-cell populations, but as yet no specific abnormality of lymphocyte phenotype or function has been found in IBD. Up-regulation of adhesion molecules on endothelial cells probably is an important first step in mucosal inflammation in IBD. Abnormal IgG and complement deposition in ulcerative colitis suggests a role for antibody-mediated injury to this disease, but not in Crohn's disease. The search for specific antibody abnormalities has focused on antineutrophil cytoplasmic antibodies: until the specific antigen recognized by IBD sera is identified and sensitive, specific and standardized tests are developed, the significance of antineutrophil cytoplasmic antibodies in IBD will remain uncertain. Biochemical studies on a wide range of potential pathologic mechanisms have further characterized the role of mucus, lysozyme, hyaluronan, phospholipases, fatty acids, lipocortin, polyamines, glycosidases, and the coagulation pathway in IBD.