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Highly Accessed Review

The role of tumor necrosis factor-alpha in systemic lupus erythematosus

Martin Aringer1* and Josef S Smolen2

Author affiliations

1 Division of Rheumatology, Department of Medicine III, University Clinical Center Carl Gustav Carus, Technical University of Dresden, Fetscherstrasse 74, 01307 Dresden, Germany

2 Department of Rheumatology, Internal Medicine III, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria

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Citation and License

Arthritis Research & Therapy 2008, 10:202  doi:10.1186/ar2341

Published: 23 January 2008

Abstract

Murine models of systemic lupus erythematosus (SLE) have shown apparently contradictory evidence in that either (a) tumor necrosis factor (TNF) expression was low and TNF administration helpful or (b) TNF was high and TNF blockade of therapeutic benefit, depending on the mouse model investigated. In fact, TNF apparently has both effects, checking autoimmunity, at least to some degree, and fostering inflammation. TNF blockade regularly, but transiently, induces or increases autoantibodies to chromatin and to phospholipids. At the same time, open-label data suggest that TNF blockade suppresses inflammatory manifestations of SLE, and long-term benefit was seen in patients with lupus nephritis. A controlled clinical trial is under way.