On the Pathogenesis Trail: What Marker B Cell Clones Tell Us about Inflammatory Bowel Disease
Author(s) -
Jonathan Braun,
Yadrira Valles-Ayoub,
Linda Berberian,
Mark Eggena,
Lynn K. Gordon,
Targan Stephan
Publication year - 1996
Publication title -
canadian journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
eISSN - 2291-2797
pISSN - 2291-2789
DOI - 10.1155/1996/198982
Subject(s) - ulcerative colitis , inflammatory bowel disease , immunology , pathogenesis , campylobacter jejuni , disease , antibody , antigen , enterocolitis , helicobacter pylori , b cell , medicine , biology , pathology , gastroenterology , genetics , bacteria
Clonal patterns of B cell activity have been recognized in inflammatory bowel disease, most notably in the immunogenetic relationship of perinuclear-antineutrophil cytoplasmic antibodies to ulcerative colitis. Conceptually, this most likely reflects the B cell response to antigens predominating at these sites of mucosal inflammation. Identification of these B cell clones and their antigenic targets may be of pathogenetic and practical importance to diagnosis and treatment. The authors describe strategies to identify such clones, based on recent advances in the characterization and detection of antibody gene products. As an example of this strategy, a clonal detection system was used to identify new marker antibodies potentially useful in the laboratory diagnosis of Crohn’s disease and ulcerative colitis. One surprising outcome of such studies is the unexpected and specific association of the B cell clonal response in Campylobacter jejuni enterocolitis and inflammatory bowel disease. By analogy to the pathogenetic role of Helicobacter pylori-induced mucositis in peptic ulcer disease, this evidence renews attention to the role of C jejuni in the initiation of ulcerative colitis and Crohn’s disease
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