 ReviewThe role of tumor necrosis factor-alpha in systemic lupus erythematosusMartin Aringer1  and Josef S Smolen2 1Division of Rheumatology, Department of Medicine III, University Clinical Center Carl Gustav Carus, Technical University of Dresden, Fetscherstrasse 74, 01307 Dresden, Germany 2Department of Rheumatology, Internal Medicine III, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria  author email corresponding author email
Arthritis Research & Therapy 2008,
10:202doi:10.1186/ar2341
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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. | 
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