Beta-adrenergic-receptor-mediated suppression of interleukin 2 receptors in human lymphocytes.
Adrenergic receptor agonists are known to attenuate the proliferative response of human lymphocytes after activation; however, their mechanism of action is unknown. Since expression of interleukin 2 (IL-2) receptors is a prerequisite for proliferation, the effect of beta-adrenergic receptor agonists on lymphocyte IL-2 receptors was studied on both mitogen-stimulated lymphocytes and IL-2-dependent T lymphocyte cell lines. In both cell types the beta-adrenergic receptor agonist isoproterenol blocked the expression of IL-2 receptors, as determined with the IL-2 receptor anti-TAC antibody. To determine the effect of beta-adrenergic agonists on expression of the high affinity IL-2 receptors, [125I]IL-2 binding studies were performed at concentrations selective for high affinity sites. No significant effect of beta-adrenergic agonists on high affinity IL-2 receptor sites could be detected. The data demonstrate that beta-adrenergic receptor agonists down-regulate IL-2 receptors primarily affecting low affinity sites.
D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D002478:Cells, Cultured; D006801:Humans; D007376:Interleukin-2 / Q000096:biosynthesis / Q000494:pharmacology; D007545:Isoproterenol / Q000494:pharmacology*; D008213:Lymphocyte Activation / Q000187:drug effects*; D011971:Receptors, Immunologic / Q000096:biosynthesis* / Q000145:classification; D015375:Receptors, Interleukin-2; D013601:T-Lymphocytes / Q000145:classification / Q000187:drug effects* / Q000276:immunology
D000318:Adrenergic beta-Agonists; D007376:Interleukin-2; D011971:Receptors, Immunologic; D015375:Receptors, Interleukin-2; D007545:Isoproterenol