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FRI0473 Autoantibody signatures of systemic lupus erythematosus (SLE) patients identified with a bead-based assay approach
  1. A. Lueking1,
  2. S. Vordenbäumen2,
  3. P. Budde1,
  4. H. Göhler1,
  5. J. Schwermann1,
  6. M. Gamer1,
  7. K. Marquardt1,
  8. A. Telaar1,
  9. D. Chamrad1,
  10. C. Theek1,
  11. B. Ostendorf2,
  12. P. Schulz-Knappe1,
  13. M. Schneider2
  1. 1Diagnostics, Protagen AG, Dortmund
  2. 2Rheumatology, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany

Abstract

Background SLE is a chronic multisystem autoimmune disease with yet unknown etiology. One hallmark of SLE is the B cell activation and the production of various autoantibodies. Differential diagnosis involves ANA screening which may yield also positive results in many connective tissue disorders and other autoimmune diseases, and may occur in normal individuals. More specific subtypes of antinuclear antibodies include anti-Smith and anti-double stranded DNA (dsDNA) antibodies. However, anti-dsDNA antibodies are present in just 70% SLE patients leaving a certain gap in diagnosis.

Objectives In this study we characterized the autoimmune signatures of SLE patients and healthy blood donors in order to identify established plus novel autoantibodies with differential abundance in serum samples of SLE patients.

Methods We used 5800 human proteins to investigate the autoantibodies present in more than 110 serum samples of SLE patients as well as healthy blood donors applying bead-based arrays (Luminex). Biostatistical analysis was performed using univariate as well as multivariate statistical algorithms.

Results In addition to the well-established clinical markers Ro52/SS-A (TRIM21), ribosomal P0, ribosomal P1, ribosomal P2, SS-A/Ro60 (TROVE2), SSB and SmB/B´ new biomarkers were identified showing high discriminatory p-values and promising sensitivity and specificity. Consequently, a small protein antigen panel consisting of four new markers plus six well-established clinical markers (Ro52/SS-A, Ro60/SS-A, ribosomal P0, ribosomal P1, ribosomal P2, and SmB/B´protein) has been defined. This panel results in an improved AUC when compared to the classification performance of the established markers alone.

Conclusions With novel biomarkers a large proportion of dsDNA AB-negative SLE patients can be addressed. The benefit of the identified marker panel for SLE diagnosis is currently evaluated in comparative analysis of other patient cohorts of ankylosing spondylitis, progressive systemic sclerosis, and rheumatoid arthritis.

Disclosure of Interest None Declared

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