On the pathogenesis trail: what marker B cell clones tell us about IBD
The pathogenesis of Crohn’s disease (CD) and ulcerative colitis (UC) is incompletely understood, but ultimately involves immune-mediated tissue damage. These diseases are associated with various immunologic abnormalities, many of which are probably secondary to inflammation1–5. CD4 T cells are widely believed to serve as key regulatory cells in tissue-destructive immune responses. In the case of inflammatory bowel disease (IBD), the response occurs in a mucosal site interfacing with the intestinal lumen. Consequently, an obvious source of target antigens are microbial products, although the identification of their role, or that of other lumenal or intrinsic mucosal cellular antigens, has yet to be established. A key step in the resolution of IBD pathogenesis and eventual treatment is the resolution of the target antigens initiating the disease. The cells which would most directly reveal the identity of these antigens are T cells. However, the low avidity of the T cell antigen receptor, and the complicated peptide/MHC II structure of its natural ligand, render these cells unsuitable for analytic studies of this important issue.
KeywordsInflammatory Bowel Disease Ulcerative Colitis Erythrocyte Membrane Protein Marker Antibody Inflammatory Bowel Disease Pathogenesis
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- 5.Elson CO. The immunology of inflammatory bowel disease. In: Kirsner JB, Sorter R, editors. Inflammatory bowel disease, 3rd edn. Philadelphia: Lea & Febiger; 1988: 97–164.Google Scholar
- 20.Berberian LS, Valles-Ayoub Y, Gordon LK, Targan SR, Braun J. Expression of a novel autoantibody defined by the VH3–15 gene in inflammatory bowel disease and Campylobacter jejuni enterocolitis. J Immunol. 1994;153:(in press)Google Scholar