Autoreactivity and altered immune responses in inflammatory bowel disease.
Inflammatory bowel disease (IBD) is a poorly understood condition that is associated with a wide variety of immunologic alterations. Because its pathogenesis is unknown, these immunologic alterations have been investigated with an eye toward unraveling the complex mechanism of injury in the bowels of these patients. There are several lines of evidence suggesting that IBD is related to immunologic events. The histopathology of active disease resembles the Arthus reaction, whereas the presence of antiepithelial cell antibodies is reminiscent of Goodpasture's disease. Antibodies against many microorganisms and autoantibodies to mucosal components are commonly found in these patients. Further, there is a marked increase in plasma cells in the lamina propria of patients with active IBD. It is important to keep these findings in perspective. No studies to date have been able to determine whether the features are entirely primary events, that is, related to the initial damage to the intestinal mucosa. If the surface mucosa is injured by an as-yet-unidentified agent, the immunologic findings in IBD may be secondary events. Nonetheless, the similarity in histopathology of the experimental immunologic models of IBD to the human disease encourages investigators to pursue the etiology of this complex disease.
Keren
D F
DF
University of Michigan, Ann Arbor.
D000818:Animals; D000917:Antibody Formation; D001323:Autoantibodies / Q000032:analysis*; D003093:Colitis, Ulcerative / Q000209:etiology / Q000276:immunology*; D003424:Crohn Disease / Q000209:etiology / Q000276:immunology*; D006801:Humans; D007111:Immunity, Cellular; D007136:Immunoglobulins / Q000032:analysis; D007413:Intestinal Mucosa / Q000276:immunology; D011453:Prostaglandins / Q000097:blood
D001323:Autoantibodies; D007136:Immunoglobulins; D011453:Prostaglandins