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Central role of nitric oxide in the pathogenesis of rheumatoid arthritis and sysemic lupus erythematosus

György Nagy12*, Agnes Koncz2, Tiffany Telarico3, David Fernandez3, Barbara Érsek2, Edit Buzás2 and András Perl3

Author Affiliations

1 Department of Rheumatology, Semmelweis University, Medical School, Budapest, Hungary

2 Department of Genetics, Cell and Immunobiology, Semmelweis University, Medical School, Budapest, Hungary

3 Departments of Medicine, Pathology, and Microbiology and Immunology, State University of New York, College of Medicine, 750 East Adams Street, Syracuse, NY 13210, USA

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Arthritis Research & Therapy 2010, 12:210  doi:10.1186/ar3045

Published: 28 June 2010


Nitric oxide (NO) has been shown to regulate T cell functions under physiological conditions, but overproduction of NO may contribute to T lymphocyte dysfunction. NO-dependent tissue injury has been implicated in a variety of rheumatic diseases, including systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). Several studies reported increased endogenous NO synthesis in both SLE and RA, and recent evidence suggests that NO contributes to T cell dysfunction in both autoimmune diseases. The depletion of intracellular glutathione may be a key factor predisposing patients with SLE to mitochondrial dysfunction, characterized by mitochondrial hyperpolarization, ATP depletion and predisposition to death by necrosis. Thus, changes in glutathione metabolism may influence the effect of increased NO production in the pathogenesis of autoimmunity.