Ileal Inflammation May Trigger the Development of GP2-Specific Pancreatic Autoantibodies in Patients with Crohn’s Disease
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 th...
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doaj-ed964679d7ff42a9892d5efd02203f142020-11-24T22:19:35ZengHindawi LimitedClinical and Developmental Immunology1740-25221740-25302012-01-01201210.1155/2012/640835640835Ileal Inflammation May Trigger the Development of GP2-Specific Pancreatic Autoantibodies in Patients with Crohn’s DiseasePolychronis Pavlidis0Ourania Romanidou1Dirk Roggenbuck2Maria G. Mytilinaiou3Faris Al-Sulttan4Christos Liaskos5Daniel S. Smyk6Andreas L. Koutsoumpas7Eirini I. Rigopoulou8Karsten Conrad9Alastair Forbes10Dimitrios P. Bogdanos11Division of Transplantation Immunology and Mucosal Biology, King’s College London School of Medicine at King’s College Hospital, London SE5 9RJ, UKDivision of Transplantation Immunology and Mucosal Biology, King’s College London School of Medicine at King’s College Hospital, London SE5 9RJ, UKFaculty of Natural Science, Lausitz University of Applied Sciences, 01968 Senftenberg, GermanyDivision of Transplantation Immunology and Mucosal Biology, King’s College London School of Medicine at King’s College Hospital, London SE5 9RJ, UKDepartment of Gastroenterology and Clinical Nutrition, University College Hospital, 250 Euston Road, London NW1 2PG, UKCellular Immunotherapy and Molecular Immunodiagnostics, Center for Research and Technology, Thessaly, 41222 Larissa, GreeceDivision of Transplantation Immunology and Mucosal Biology, King’s College London School of Medicine at King’s College Hospital, London SE5 9RJ, UKDivision of Transplantation Immunology and Mucosal Biology, King’s College London School of Medicine at King’s College Hospital, London SE5 9RJ, UKDepartment of Medicine, University of Thessaly Medical School, Viopolis, Larissa 41110, GreeceInstitute of Immunology, Technical University Dresden, Fetscherstrasse 74, 01307 Dresden, GermanyDepartment of Gastroenterology and Clinical Nutrition, University College Hospital, 250 Euston Road, London NW1 2PG, UKDivision of Transplantation Immunology and Mucosal Biology, King’s College London School of Medicine at King’s College Hospital, London SE5 9RJ, UKWhy 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 (P<0.001). Only 5 CDs with L2 had anti-GP2 antibodies, compared to 54/180 (30.0%, P=0.0128) 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 (P<0.001). 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.http://dx.doi.org/10.1155/2012/640835 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Polychronis Pavlidis Ourania Romanidou Dirk Roggenbuck Maria G. Mytilinaiou Faris Al-Sulttan Christos Liaskos Daniel S. Smyk Andreas L. Koutsoumpas Eirini I. Rigopoulou Karsten Conrad Alastair Forbes Dimitrios P. Bogdanos |
spellingShingle |
Polychronis Pavlidis Ourania Romanidou Dirk Roggenbuck Maria G. Mytilinaiou Faris Al-Sulttan Christos Liaskos Daniel S. Smyk Andreas L. Koutsoumpas Eirini I. Rigopoulou Karsten Conrad Alastair Forbes Dimitrios P. Bogdanos Ileal Inflammation May Trigger the Development of GP2-Specific Pancreatic Autoantibodies in Patients with Crohn’s Disease Clinical and Developmental Immunology |
author_facet |
Polychronis Pavlidis Ourania Romanidou Dirk Roggenbuck Maria G. Mytilinaiou Faris Al-Sulttan Christos Liaskos Daniel S. Smyk Andreas L. Koutsoumpas Eirini I. Rigopoulou Karsten Conrad Alastair Forbes Dimitrios P. Bogdanos |
author_sort |
Polychronis Pavlidis |
title |
Ileal Inflammation May Trigger the Development of GP2-Specific Pancreatic Autoantibodies in Patients with Crohn’s Disease |
title_short |
Ileal Inflammation May Trigger the Development of GP2-Specific Pancreatic Autoantibodies in Patients with Crohn’s Disease |
title_full |
Ileal Inflammation May Trigger the Development of GP2-Specific Pancreatic Autoantibodies in Patients with Crohn’s Disease |
title_fullStr |
Ileal Inflammation May Trigger the Development of GP2-Specific Pancreatic Autoantibodies in Patients with Crohn’s Disease |
title_full_unstemmed |
Ileal Inflammation May Trigger the Development of GP2-Specific Pancreatic Autoantibodies in Patients with Crohn’s Disease |
title_sort |
ileal inflammation may trigger the development of gp2-specific pancreatic autoantibodies in patients with crohn’s disease |
publisher |
Hindawi Limited |
series |
Clinical and Developmental Immunology |
issn |
1740-2522 1740-2530 |
publishDate |
2012-01-01 |
description |
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 (P<0.001). Only 5 CDs with L2 had anti-GP2 antibodies, compared to 54/180 (30.0%, P=0.0128) 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 (P<0.001). 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. |
url |
http://dx.doi.org/10.1155/2012/640835 |
work_keys_str_mv |
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