Immunology of inflammatory bowel disease

Multiple studies have examined the T cell repertoire of peripheral blood and mucosal lymphocytes in patients with inflammatory bowel disease (IBD), and evidence of expansion of clonal populations of T cells has been found in both diseases, suggesting that the abnormal immune responses may be driven by specific antigens. Studies of cytokine production in IBD has added further evidence that Crohn's disease and ulcerative colitis differ, with Crohn's disease being characterized by high expression of interferon gamma and ulcerative colitis by high expression of interleukin-5 in activated mucosal lymphocytes. Antigen-presenting cells in IBD are activated and express surface molecules that may play an important role in costimulation and in specific mechanisms of tissue injury and repair. Further evidence for a possible immunogenetic basis of IBD has emerged from new studies defining associations with HLA molecules and TAP genes. Possible new roles for the epithelium in modulating inflammatory responses have been demonstrated by the presence of high levels of inducible nitric oxide synthase in inflamed epithelium in IBD. Antibodies and autoantibodies continue to be studied as potential markers of patient subgroups and to elucidate underlying pathogenesis.