Regulatory and pathogenetic mechanisms of autoantibodies in SLE

Abstract

In the 53 years since the discovery of anti-DNA autoantibodies in lupus , recalcitrant questions have been pondered and possible answers have been debated. The discovery of anti-DNA autoantibodies presented many puzzles: How is immunological tolerance to native B-form DNA broken? What elicits characteristic systemic lupus erythematosus (SLE) autoantibodies? Which of the diverse anti-nuclear reactivities are pathogenic? What is the role of autoantibodies in the clinical presentation of disease? How do genetic predisposition and environmental triggers contribute to SLE? These questions were brought into focus by Professor David Stollar in an introductory presentation to an intense, three-day meeting set among the rugged and inspiring scenery of the Norwegian arctic coastline (the Scientific Program is included as supplemental File 1). Other participants presented and discussed topics directed to understanding the origin and clinico-pathological impact of autoantibodies to chromatin and phospholipid antigens. In the following, several aspects of the workshop are discussed.

Keywords::

• Systemic lupus erythematosus
• autoantibodies
• anti-DNA antibodies
• B cell regulation
• apoptosis

Acknowledgements

The authors gratefully acknowledge the written summaries of the presented research and figures that were prepared and submitted by the workshop participants for use in this brief review (see Supplementary Table I for the program of the workshop). M.R. acknowledges the Lupus Research Institute of New York City and the Dana Foundation Program in Human Immunology for support of research.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.