putative autoantigen in ulcerative colitis

The intestinal expression pattern and general tissue distribution of the M. 40 kD putative epithelial autoantigen in ulcerative colitis were re-examined by in situ two and three colour immunofluorescence staining including the murine monoclonal antibody 7E,2H,2. The intestinal distribution was also compared with the epithelial codeposition of IgGI and activated complement (C3b and terminal complement complex) seen selectively in ulcerative colitis. The M, 40 kD antigen was found for the first time in goblet cells of normal terminal ileum and proximal colon but not in rectal goblet cells. By contrast, colonic enterocytes expressed this antigen apically with increasing intensity in a distal direction, expanding to intense cytoplasmic expression in rectal enterocytes. The antigen was also expressed by the epithelium of the fallopian tubes, major bile ducts, gall bladder, and epidermis but not by proximal gastrointestinal tract epithelium or 13 other extragastrointestinal organs. Activated complement and IgGI often colocalised with the M, 40 kD antigen apically on the surface epithelium in active ulcerative colitis but not in Crohn's disease. Our results support the idea that an autoimmune response to this antigen, leading to complement activation mediated by IgGI, is a possible pathogenetic mechanism for epithelial damage and persistent inflammation in ulcerative colitis. (Gut 1993; 34:650-657) Laboratory for Immunohistochemistry and Immunopathology, Institute of Pathology, University of Oslo, The National Hospital, Rikshospitalet, Oslo, Norway T S Halstensen P Brandtzaeg Division of Gastroenterology and Hepatology, Department of Medicine, University of Medicine and Dentistry of New JerseyRobert Wood Johnson Medical School, New Brunswick, New Jersey, USA KM Das Correspondence to: Dr T S Halstensen, LIIPAT, Rikshospitalet, N-0027 Oslo, Norway. Accepted for publication 7 September 1992 Immunoglobulin GI (IgGl), along with activated early (Clq, C4c, C3b) and late (terminal complement complex) components of the complement cascade, is deposited on the apical face of the colonic epithelium in active ulcerative colitis lesions but not in Crohn's colitis. 2 This disparity suggests that IgGI autoantibodies to antigen(s) associated with the epithelial brush border initiate epithelial complement attack in ulcerative