The role of nitric oxide in abnormal T cell signal transduction in systemic lupus erythematosus.

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.

• Authors: Gyorgy Nagy, Andras Perl
• Journal: Clinical immunology (Orlando, Fla.) (Clin Immunol) 2006 Feb-Mar Vol. 118 Issue 2-3 Pg. 145-51 ISSN: 1521-6616 [Print] United States
• PMID: 16406340 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Nitric Oxide

Topics

• Animals
• Humans
• Lupus Erythematosus, Systemic (immunology, metabolism, pathology)
• Nitric Oxide (physiology)
• Signal Transduction (immunology)
• T-Lymphocytes (metabolism, pathology)