The role of tumor necrosis factor-alpha in systemic lupus erythematosus
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
Citation and License
Arthritis Research & Therapy 2008, 10:202 doi:10.1186/ar2341Published: 23 January 2008
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.