Abstract
The expression of beta-adrenergic receptors on murine lymphocytes stimulated with concanavalin A was studied. A decrease in beta-adrenoceptor number on T lymphocytes and a diminished response to specific agonist stimulation at the peak of proliferation was found. The blockade of cell proliferation by tyrosine kinases or protein kinase C inhibitors reversed the decrease in beta-adrenoceptor number. PMA plus ionophore or interleukin-2 but not PMA alone were able to induce beta-adrenoceptor down-regulation accompanying cellular proliferation. These results showed that the intracellular signals triggered during lymphocyte activation are involved in beta-adrenoceptor down-regulation and it would represent the loss of a mechanism that exerts negative neuroimmune control of cellular proliferation.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
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Animals
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Calcimycin / pharmacology
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Concanavalin A / pharmacology
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Cyclic AMP / metabolism
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Down-Regulation
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Genistein
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In Vitro Techniques
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Interleukin-2 / metabolism
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Intracellular Fluid / metabolism
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Isoflavones / pharmacology
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Isoquinolines / pharmacology
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Lymphocyte Activation / physiology*
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Mice
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Mice, Inbred BALB C
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Neuroimmunomodulation
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Piperazines / pharmacology
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Protein Kinase Inhibitors
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Protein-Tyrosine Kinases / antagonists & inhibitors
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Receptors, Adrenergic, beta / immunology
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Receptors, Adrenergic, beta / metabolism*
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Signal Transduction
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Sulfonamides*
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T-Lymphocytes / drug effects
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T-Lymphocytes / immunology*
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T-Lymphocytes / metabolism*
Substances
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Interleukin-2
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Isoflavones
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Isoquinolines
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Piperazines
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Protein Kinase Inhibitors
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Receptors, Adrenergic, beta
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Sulfonamides
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Concanavalin A
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Calcimycin
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1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
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N-(2-guanidinoethyl)-5-isoquinolinesulfonamide
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Genistein
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Cyclic AMP
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Protein-Tyrosine Kinases