title: Evidence of Crohn's disease-related anti-glycoprotein 2 antibodies in patients with celiac disease.
abstract: BACKGROUND
  Autoantibodies to exocrine-pancreatic glycoprotein 2 (anti-GP2) are Crohn's disease (CD) markers. However, CD-specific antibodies have also been found in celiac-disease (CeD) patients, in which type 1 diabetes-specific autoantibodies against endocrine pancreatic targets can be present. We investigated whether anti-GP2 are also present in CeD, a disease like CD which is also characterised by intestinal mucosal inflammation with barrier impairment.
  
  
  METHODS
  Antibodies against GP2, tissue transglutaminase (tTG), deamidated gliadin (dGD), glutamic decarboxylase (GAD), and islet antigen-2 (IA2) were tested in sera from 73 CD patients, 90 blood donors (BD), and 79 (58 de novo) CeD patients (2 consecutive sera were available from 40 patients).
  
  
  RESULTS
  IgA and/or IgG anti-GP2 were found in 15/79 (19.0%) CeD patients on at least one occasion, in 25/73 (34.2%) CD patients, and in 4/90 (4.4%) BD (CeD vs. CD, p=0.042; BD vs. CeD and CD, p<0.001, respectively). Amongst the 58 de novo CeD patients, anti-GP2 IgA and/or IgG were present in 11 (19.0%). Anti-GP2 IgA was significantly less prevalent in CeD compared with CD (p=0.004). Anti-GP2 IgA and IgG in CD patients demonstrated a significantly higher median level compared to patients with CeD (p<0.001, p=0.008, respectively). IgA anti-GP2 levels correlated significantly with IgA anti-tTG and anti-dGD levels in CeD Spearman's coefficient of rank correlation (ρ)=0.42, confidence interval (CI): 0.26-0.56, p<0.001; ρ=0.54, CI 0.39-0.65, p<0.001, respectively.
  
  
  CONCLUSIONS
  The presence of anti-GP2 in CeD patients supports the notion that loss of tolerance to GP2 can probably be a manifestation of an autoinflammatory process in this intestinal disorder.
authors.forename: Dirk
authors.initials: D
authors.lastname: Roggenbuck
authors.forename: Severine
authors.initials: S
authors.lastname: Vermeire
authors.forename: Ilse
authors.initials: I
authors.lastname: Hoffman
authors.forename: Dirk
authors.initials: D
authors.lastname: Reinhold
authors.forename: Peter
authors.initials: P
authors.lastname: Schierack
authors.forename: Alexander
authors.initials: A
authors.lastname: Goihl
authors.forename: Ulrike
authors.initials: U
authors.lastname: von Arnim
authors.forename: Gert
authors.initials: G
authors.lastname: De Hertogh
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Polymeros
authors.forename: Dimitrios P
authors.initials: DP
authors.lastname: Bogdanos
authors.forename: Xavier
authors.initials: X
authors.lastname: Bossuyt
mesh_terms: D000293:Adolescent; D000328:Adult; D001323:Autoantibodies / Q000097:blood / Q000276:immunology; D016022:Case-Control Studies; D002446:Celiac Disease / Q000097:blood* / Q000276:immunology*; D002648:Child; D015331:Cohort Studies; D003424:Crohn Disease / Q000276:immunology*; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology; D005260:Female; D005500:Follow-Up Studies; D058851:GPI-Linked Proteins / Q000276:immunology*; D006801:Humans; D007070:Immunoglobulin A / Q000097:blood* / Q000276:immunology; D007074:Immunoglobulin G / Q000097:blood* / Q000276:immunology; D008297:Male; D013997:Time Factors; D055815:Young Adult
chemical_list: D001323:Autoantibodies; C489339:GP2 protein, human; D058851:GPI-Linked Proteins; D007070:Immunoglobulin A; D007074:Immunoglobulin G