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Gastroenterology Research and Practice
Volume 2013, Article ID 683824, 7 pages
Review Article

The Novel Crohn's Disease Marker Anti-GP2 Antibody Is Associated with Ileocolonic Location of Disease

1R/D, Medipan GmbH, 15827 Dahlewitz/Berlin, Germany
2Immunology Department, King Hussein Medical Center, Amman 11855, Jordan
3University of Jordan, Amman 11942, Jordan
4Department of Pediatrics, Polytechnic University of Marche, 60123 Ancona, Italy
5Department of Gastroenterology, “Ospedali Riuniti” University Hospital, 60020 Ancona, Italy
6Institute of Immunology, Technical University, 01307 Dresden, Germany
7Division of Transplantation Immunology and Mucosal Biology, Institute of Liver Studies, King’s College London School of Medicine at King’s College Hospital, Denmark Hill Campus, London SE5 9RJ, UK
8Faculty of Natural Sciences, Lausitz University of Applied Sciences, 01968 Senftenberg, Germany
9Central Analytical Laboratory, “Ospedali Riuniti” University Hospital, 60020 Ancona, Italy

Received 11 February 2013; Accepted 19 March 2013

Academic Editor: Devendra Amre

Copyright © 2013 Valentina Somma 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.


Crohn's disease (CD) is an inflammatory bowel disease (IBD) that can affect the whole gastrointestinal tract. The ileocolonic variant of CD, an inflammation of both the ileum and the large intestine, accounts for up to 50% of the cases with CD, whereas Crohn's ileitis affecting the ileum is diagnosed in about 30%. Crohn's colitis, which is confined to the large intestine and accounts for the remaining 20%, is difficult to distinguish from the large bowel inflammation seen in patients with ulcerative colitis (UC). The pathogenesis of CD is not yet completely understood. Autoimmunity is one factor that can partake in the triggering or modulation of inflammatory processes in IBD. The major zymogen-granule membrane glycoprotein 2 (GP2) has been recently identified as a major autoantigenic target in CD. Interestingly, GP2 is mainly expressed in the pancreas and has also been demonstrated to be a membrane-anchored receptor of microfold cells in the follicle-associated epithelium. Remarkably, GP2 is overexpressed at the site of CD inflammation in contrast to the one in UC. By utilizing novel enzyme-linked immunosorbent assays for the detection of GP2-specific IgA and IgG, the loss of tolerance to GP2 has been associated with a specific clinical phenotype in CD, in particular with the ileocolonic location of the disease.