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Clinical and Developmental Immunology
Volume 2012 (2012), Article ID 640835, 8 pages
http://dx.doi.org/10.1155/2012/640835
Clinical Study

Ileal Inflammation May Trigger the Development of GP2-Specific Pancreatic Autoantibodies in Patients with Crohn’s Disease

1Division of Transplantation Immunology and Mucosal Biology, King’s College London School of Medicine at King’s College Hospital, London SE5 9RJ, UK
2Department of Gastroenterology and Clinical Nutrition, University College Hospital, 250 Euston Road, London NW1 2PG, UK
3Cellular Immunotherapy and Molecular Immunodiagnostics, Center for Research and Technology, Thessaly, 41222 Larissa, Greece
4Faculty of Natural Science, Lausitz University of Applied Sciences, 01968 Senftenberg, Germany
5GA Generic Assays GmbH, L.-Erhard-Ring 3, Dahlewitz, 15827 Berlin, Germany
6Department of Medicine, University of Thessaly Medical School, Viopolis, Larissa 41110, Greece
7Institute of Immunology, Technical University Dresden, Fetscherstrasse 74, 01307 Dresden, Germany

Received 22 June 2012; Accepted 7 September 2012

Academic Editor: Xavier Bossuyt

Copyright © 2012 Polychronis Pavlidis et al. 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.

Abstract

Why zymogen glycoprotein 2 (GP2), the Crohn’s disease (CD)-specific pancreatic autoantigen, is the major target of humoral autoimmunity in inflammatory bowel diseases (IBD) is uknown. Recent evidence demonstrates that GP2 is also present on the apical surface of microfold (M) intestinal cells. As the colon lacks GP2-rich M cells, we assumed that patients with colonic CD are seronegative for anti-GP2. Anti-GP2 antibodies were tested in 225 CDs, including 45 patients with colonic location (L2), 45 with terminal ileum (L1) and 135 with ileocolonic involvement; 225 patients with ulcerative colitis (UC) were also tested. Anti-GP2 reactivity was detected in 59 (26.2%) CDs and 15 (6.7%) UCs . Only 5 CDs with L2 had anti-GP2 antibodies, compared to 54/180 (30.0%, ) of the CDs with L1 and L3. Anti-GP2 antibody positive CD patients had higher ASCA titres compared to seronegative cases. Amongst the 128 CD patients with previous surgical intervention, 45 (35.0%) were anti-GP2 antibody positive compared to 14/97 (14.0%) without surgical . Our data support the assumption that ileal inflammation is required for the development of anti-GP2 antibodies in CD, and suggest that the intestine rather than the pancreatic juice is the antigenic source required for the initiation of anti-GP2 antibodies.