Back to Search
Start Over
Mitochondrial dysfunction in T cells of patients with systemic lupus erythematosus.
- Source :
-
International reviews of immunology [Int Rev Immunol] 2004 May-Aug; Vol. 23 (3-4), pp. 293-313. - Publication Year :
- 2004
-
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 (Delta Psi(m)) 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.
- Subjects :
- Adenosine Triphosphate biosynthesis
Apoptosis
Humans
Interleukin-10 physiology
Interleukin-12 physiology
Lupus Erythematosus, Systemic metabolism
Lymphocyte Activation
Membrane Potentials
Mitochondria immunology
Reactive Oxygen Species metabolism
Signal Transduction
T-Lymphocytes cytology
T-Lymphocytes metabolism
Lupus Erythematosus, Systemic immunology
Mitochondria metabolism
T-Lymphocytes immunology
Subjects
Details
- Language :
- English
- ISSN :
- 0883-0185
- Volume :
- 23
- Issue :
- 3-4
- Database :
- MEDLINE
- Journal :
- International reviews of immunology
- Publication Type :
- Academic Journal
- Accession number :
- 15204090
- Full Text :
- https://doi.org/10.1080/08830180490452576