ReviewClinical immunology (Orlando, Fla.)
The role of nitric oxide in abnormal T cell signal transduction in systemic lupus erythematosus.
Review in Clinical immunology (Orlando, Fla.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 16 citations in OpenAlex.
- Identifying independent causal cell types for human diseases and risk variants.Cell genomics · 2026Article
- Redox Pathogenesis in Rheumatic Diseases.ACR open rheumatology · 2024Review
- Immunometabolic disorders in the pathogenesis of systemic lupus erythematosus.Postepy dermatologii i alergologii · 2019Review
- Article
- Inducible nitric oxide synthase inhibitor SD-3651 reduces proteinuria in MRL/lpr mice deficient in the NOS2 gene.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2008Article
- Association of reactive oxygen and nitrogen intermediate and complement levels with apoptosis of peripheral blood mononuclear cells in lupus patients.Arthritis and rheumatism · 2007Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by production of antinuclear autoantibodies and diverse array of clinical manifestations. T cells from patients with SLE have been shown to be activated in vivo and provide help to autoreactive B cells. Lupus T cells exhibit enhanced spontaneous and diminished activation-induced apoptosis and predisposition to necrosis. Persistent mitochondrial hyperpolarization and ATP depletion - associated with significantly increased mitochondrial mass - characterize T lymphocyte dysfunction in SLE. In addition to cell death abnormalities, mitochondrial dysfunction is associated with altered signal transduction through the T cell receptor and Ca2+ fluxing. Exposure of normal T cell to nitric oxide induces mitochondrial hyperpolarization and biogenesis and regenerates the Ca2+ signaling profile of lupus T cells. This article reviews a novel understanding of the role of nitric oxide in signal transduction and cell death abnormalities in SLE.
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Registered trials
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