@article{3088464,
    title = "Evidence of Crohn's disease-related anti-glycoprotein 2 antibodies in patients with celiac disease",
    author = "Roggenbuck, D. and Vermeire, S. and Hoffman, I. and Reinhold, D. and Schierack, P. and Goihl, A. and Von Arnim, U. and De Hertogh, G. and Polymeros, D. and Bogdanos, D.P. and Bossuyt, X.",
    journal = "Clinical Chemistry and Laboratory Medicine (CCLM)",
    year = "2015",
    volume = "53",
    number = "9",
    pages = "1349-1357",
    publisher = "Walter de Gruyter GmbH",
    doi = "10.1515/cclm-2014-0238",
    keywords = "autoantibody;  bispecific antibody;  gliadin antibody;  glutamate decarboxylase;  glycoprotein 2 antibody;  immunoglobulin A antibody;  immunoglobulin G antibody;  protein antibody;  protein glutamine gamma glutamyltransferase antibody;  unclassified drug;  autoantibody;  glycosylphosphatidylinositol anchored protein;  GP2 protein, human;  immunoglobulin A;  immunoglobulin G, adolescent;  adult;  antibody blood level;  Article;  blood donor;  celiac disease;  child;  comparative study;  Crohn disease;  enzyme linked immunosorbent assay;  female;  human;  immunological tolerance;  major clinical study;  male;  priority journal;  blood;  case control study;  celiac disease;  cohort analysis;  Crohn disease;  follow up;  immunology;  insulin dependent diabetes mellitus;  time factor;  young adult, Adolescent;  Adult;  Autoantibodies;  Case-Control Studies;  Celiac Disease;  Child;  Cohort Studies;  Crohn Disease;  Diabetes Mellitus, Type 1;  Female;  Follow-Up Studies;  GPI-Linked Proteins;  Humans;  Immunoglobulin A;  Immunoglobulin G;  Male;  Time Factors;  Young Adult",
    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. © 2015 by De Gruyter."
}