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Canadian Journal of Gastroenterology
Volume 10, Issue 2, Pages 115-119

On the Pathogenesis Trail: What Marker B Cell Clones Tell Us about Inflammatory Bowel Disease

Jonathan Braun, Yadrira Valles-Ayoub, Linda Berberian, Mark Eggena, Lynn K Gordon, and Targan Stephan

Departments of Pathology, Ophthalmology and Medicine, UCLA School of Medicine, and IBD Research Center, Cedars-Sinai Medical Center, Los Angeles, California, USA

Copyright © 1996 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.