Abstract

Autoantibodies may be found years before an autoimmune disease becomes clinically apparent. For systemic lupus erythematosus (SLE), those to RNA-binding proteins, to phospholipids, and to double-stranded DNA, in particular, have been found in sera of SLE patients years before the diagnosis was made. New data now show in an unbiased way that, in patients with early SLE, no single antibody class or specificity is associated with progression to SLE. Rather, an increasing number of autoantibody specificities, such as to thyroid antigens, was observed in patients progressing. This points to more generalized B cell autoreactivity during progression to SLE, underlying lupus disease manifestations.

Highlights

  • Autoantibodies may be found years before an autoimmune disease becomes clinically apparent

  • In a previous issue of Arthritis Research & Therapy, Nancy Olsen and colleagues from the Penn State Hershey Medical Center and the University of Texas Southwestern Medical Center present an analysis of a wide range of autoantibodies in patients with ‘incomplete’ systemic lupus erythematosus (SLE) [1]

  • Out of 22 patients, only 3 developed additional SLE criteria during a follow-up of 3.8 ± 0.6 years. These three patients showed some possible differences in their serology. They had higher titers of antibodies to hemocyanin and PL-7, and somewhat higher levels of antibodies to thyroglobulin, thyroid peroxidase, proliferating cell nuclear antigen, β2-microglobulin, and C1q, not all of which are typically associated with SLE

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Summary

Introduction

Autoantibodies may be found years before an autoimmune disease becomes clinically apparent. In a previous issue of Arthritis Research & Therapy, Nancy Olsen and colleagues from the Penn State Hershey Medical Center and the University of Texas Southwestern Medical Center present an analysis of a wide range of autoantibodies in patients with ‘incomplete’ SLE [1]. Within the Dallas Regional Autoimmune Disease registry (DRADR) cohort, they have followed patients who, with one exception, did not fulfill American College of Rheumatology criteria for systemic lupus erythematosus (SLE) at baseline using an autoantigen array.

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