Lipoic acid stimulates cAMP production in T lymphocytes and NK cells |
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Authors: | Schillace R V Pisenti N Pattamanuch N Galligan S Marracci G H Bourdette D N Carr D W |
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Affiliation: | Portland Veterans Affairs Medical Center and Department of Neurology, Oregon Health & Science University, Portland, OR 97239, USA. |
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Abstract: | The anti-oxidant lipoic acid (LA) potently suppresses clinical and pathologic disease in the animal model of multiple sclerosis, experimental autoimmune encephalomyelitis, by inhibiting the migration of pathogenic T cells to the spinal cord. The mechanism by which this occurs is largely unknown. In this report we demonstrate that LA induces increases in cyclic AMP, a known immunosuppressant, in human T cells. The increase in cAMP is associated with increased adenylyl cyclase activity and is partially blocked by prostanoid receptor antagonists. We present evidence that LA also stimulates cAMP production in natural killer (NK) cells. This novel mechanism of action is highly relevant to the immunomodulatory effects of LA and provides further support for the study of LA as a therapeutic agent for multiple sclerosis and other autoimmune diseases. |
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Keywords: | AC, adenylyl cyclase cAMP, cyclic AMP DHLA, dihydrolipoic acid DMLA, dimethyl lipoic acid IBMX, isobutylmethylxanthine LA, lipoic acid LPM, lipoamide (DL 6,8-thioctic acid amide) NK, natural killer cell PDE, phosphodiesterase PGE2, prostaglandin E2 PGD2, prostaglandin D2 PKA, protein kinase A |
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