Autoimmunity in Inflammatory Bowel Disease

KM DAS. Autoimmunity in inflammatory bowel disease. Can J Gastroenterol 1993;7(2):102-109. Autoimmune injury to the colonic epithelium has been a favoured hypothesis ever since circulating anticolon antibodies were first demonstrated in patients with inflammatory bowel disease (IBO). There is some evidence that anticolon antibodies present in the scrn from patients with ulcerative colitis, but not Crohn's disease, may injure epithelial cells by antibody-dependent cellular cytotoxicity (ADCC) . The ADCC correlated with the disease state in ulcerative colitis and disappeared following total colectomyRecent studies also demonstrated specific immunoglobulin (lg) G deposition along with activated complement components on colonic epithelium in ulcerative colitis and not in Crohn's disease, suggesting a role of anti-epithelial antihody causing cellular damage. The mucosal B cells in ulcerative colitis produce anticolon antibodies. Antineutrophil cytoplasmic antibody in patients with ulcerative colitis is intriguing and identification of the immunoreactive antigen from the neutrophils may explain its association with ulcerative colitis. Detection of intestinal mucosa( T cells reactive against epithelial cell-associated components also supports the existence of cytotoxic cells aimed at intestinal cells. The isolation of colon-bound IgG antibody in ulcerative colitis directed towards a unique colonic antigen, molecular weight fraction (Mr) 40K protein (P-40) suggests a specific form of autoimmunity in ulcerative colitis. P-40 is expressed in colonic epithelium and not in 13 other epithelial organs including other parts of the gastrointestinal tract, However, extraintestinal organs such as skin and biliary epithelium (organs commonly affected in ulcerative colitis) have a unique epitope shared with colonic epithelium. Anti-P-40 antibodies are present in the circulation of patients with ulcerative colitis and peripheral blood lymphocytes show proliferative response to the colon extract enriched in P-40. Recent studies demonstrated amplified lgG 1 antibody in the circulation (as well as in situ) bound to the colonic mucosa! epithelium along with activated complement products in patients with ulcerative colitis and not in Crohn's disease. This lgG 1 autoantibody response appears to be predominantly directed to P-40. (Pour resume, voir page 103)