MITOCHONDRIAL DYSFUNCTION IN T CELLS OF PATIENTS WITH SYSTEMIC LUPUS ERYTHEMATOSUS |
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| Authors: | ANDRAS PERL PETER GERGELY JR. KATALIN BANKI |
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| Affiliation: | 1. Department of Medicine and Department of Microbiology and Immunology, State University of New York, Upstate Medical University, College of Medicine, Syracuse, New York, USAperla@upstate.edu;3. Department of Medicine, State University of New York, Upstate Medical University, College of Medicine, Syracuse, New York, USA;4. Department of Pathology, State University of New York, Upstate Medical University, College of Medicine, Syracuse, New York, USA |
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| Abstract: | Activation, proliferation, or programmed cell death of T lymphocytes are dependent on controlled reactive oxygen intermediates (ROI) production and ATP synthesis in mitochondria. The mitochondrial transmembrane potential (ΔΨm) also plays a decisive role in cell survival by controlling activity of redox-sensitive caspases. T lymphocytes of patients with systemic lupus erythematosus (SLE) exhibit mitochondrial hyperpolarization, increased ROI production, diminished intracellular glutathione levels, cytoplasmic alkalinization, and ATP depletion that mediate enhanced spontaneous and diminished activation-induced apoptosis and sensitize lupus T cells to necrosis. These redox and metabolic checkpoints represent novel targets for pharmacological intervention in SLE. |
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| Keywords: | human lupus signal transduction |
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