Prevalence Of Antibodies To Glycoprotein 2 In Patients With Spondyloarthropathies

Background and objectives Autoimmune diseases are characterised by tissue damage and loss of function due to an immune response that is directed against specific organs. Together with the gut-associated lymphoid tissue and the neuroendocrine network, the intestinal epithelial barrier, with its intercellular tight junctions, controls the equilibrium between tolerance and immunity to non-self antigens. Pancreatic zymogen granule protein 2 Glycoprotein 2 (GP2) has been identified as a major autoantigenic target of the so-called pancreatic antibodies. Antibodies to GP2 have demonstrated diagnostic significance for Crohn’s disease. Anti-GP2 autoantibodies are detected in 25–30% of patients with CD and in 5–12% of patients with UC. There are certain relationships in pathgenesis and clinical course of inflammatory bowel diseases and spondyloarthropathies. The aim of our study is to investigate the prevalence of anti-GP2 in patients with SpA and evaluate the potential impact in relationships between gut inflammation and development the systemic autoimmune process. Materials and methods We studied 87 patients with SpA (64 patients with ankylosing spondylitis (AS), 23 – with psoriatic arthritis (PsA). As healthy controls 160 adult blood donors were included. All patients are fulfilled respective latest classification criteria. Levels of anti-GP2 antibodies (IgA and IgG classes) have been detected by ELISA, employing recombinant human GP2 (Medipan GmbH, Germany). Cut-off levels, determined by manufactures, are ≥20 U/ml. Results Anti-GP2 IgA were more prevalent in SpA (39/87, 44.82%) in controls (6/160, 3.75%) (p Anti-GP2 IgG were more prevalent in SpA (17/87, 19.54%) patients than in controls (4/160, 2.5%) (p Conclusions Anti-GP2 antibodies, considering as a novel CD-specific markers, are found to be positive in about 44% of patients with SpA. Moreover, the highest prevalence anti-GP2 IgA was observed in PsA patients. These data may help to find new interrelationships between gut inflammation and the development of autoimmune diseases.