Immunology of inflammatory bowel disease.

Although the aetiology of ulcerative colitis and Crohn's disease remain unknown, immunological effector mechanisms become activated within the inflamed mucosa and may be responsible for the pathogenesis of chronic disease. There is an increased production of immunoglobulin within the mucosa, some of which has specificity for bacterial antigens, and complement activation occurs during exacerbation of the disease. Lymphocytes isolated from peripheral blood, or from the intestinal mucosa, are cytotoxic to colonic epithelial cells in vitro; a reaction which can be modulated by serum factors and bacterial antigens. Within the mucosa, there are increased populations of T lymphocytes although there is no change in the ratio of helper- to suppressor-cells as defined by phenotype. Studies of immunoregulatory control have shown that there may be alterations in the modulation of the local immune response, especially during active disease, although it is not clear whether these changes are primary or merely secondary to inflammation. It is posulated that many of the humoral and cellular responses to gut-associated antigens occur as a result of increased antigen absorption, increased presentation of antigen to the immune system due to the expression of Class II antigens by the inflamed epithelium and altered immuno-regulatory control.