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Raised levels of anti-glucose-6-phosphate isomerase IgG in serum and synovial fluid from patients with inflammatory arthritis
  1. M Schaller1,
  2. W Stohl2,
  3. S M Tan2,
  4. V M Benoit1,
  5. D M Hilbert3,
  6. H J Ditzel1,4
  1. 1Department of Immunology, Scripps Research Institute, La Jolla, CA 92037, USA
  2. 2Division of Rheumatology, Los Angeles County + University of Southern California Medical Center and Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA
  3. 3Human Genome Sciences, Inc, Rockville, MD 20850, USA
  4. 4Medical Biotechnology Centre, University of Southern Denmark, 5000 Odense C, Denmark
  1. Correspondence to:
    Professor H J Ditzel
    Medical Biotechnology Centre, University of Southern Denmark, Winsloewparken 25, 5000 Odense C, Denmark; hditzelhealth.sdu.dk

Abstract

Background: In K/BxN mice, anti-glucose-6-phosphate isomerase (GPI) antibodies (Abs) are arthritogenic, and their transfer into naïve mice induces arthritis. Anti-GPI Abs develop in many human patients with RA and are associated with more severe forms of the disease.

Objective: To elucidate the serum and synovial fluid (SF) anti-GPI IgG profiles among different patient groups with a variety of arthritides.

Methods: Blood and SF obtained concomitantly from 91 patients with clinically well defined arthritis were tested for concentrations of total anti-GPI IgG, anti-GPI IgG subclasses, B lymphocyte stimulator (BLyS), and APRIL by ELISA.

Results: Anti-GPI IgG was detected in sera and SF of patients with many arthritic diseases, but was preferentially associated with inflammatory arthritis, in general, and RA, in particular. The anti-GPI IgG subclass usage was skewed and varied among the different arthritic disease groups. Inverse correlations between serum levels of BLyS and anti-GPI IgG and positive correlations between serum levels of APRIL and anti-GPI IgG were seen among immune based arthritic patients and patients with RA but not among non-immune based patients. No correlations were found in SF from any group of arthritic patients.

Conclusion: Raised circulating anti-GPI Abs are not unique to patients with RA but are present in many patients with inflammatory arthritis. The difference in anti-GPI IgG subclass usage among disease groups may influence effector function and disease outcome. The inverse correlation between serum BLyS and anti-GPI IgG levels suggests that anti-GPI B cells may be regulated differently from other autoantibody producing B cells. Anti-GPI Abs may serve a pathogenic function in humans by promoting the maintenance of existing disease.

  • Abs, antibodies
  • AP, alkaline phosphatase
  • BLyS, B lymphocyte stimulator
  • Crys, crystal induced arthritis
  • ELISA, enzyme linked immunosorbent assay
  • GPI, glucose-6-phosphate isomerase
  • OA, osteoarthritis
  • PBS, phosphate buffered saline
  • RA, rheumatoid arthritis
  • RF, rheumatoid factor
  • SLE, systemic lupus erythematosus
  • SpA, spondyloarthropathies
  • Tr, traumatic arthritis
  • IgG subclasses
  • glucose-6-phosphate isomerase
  • autoantibodies
  • rheumatoid arthritis

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