β2-Adrenergic Receptor Stimulation-Induced Immunosuppressive Effects Possibly through Down-Regulation of Co-Stimulatory Molecules, ICAM-1, CD40 and CD14 on Monocytes
Open Access
- 1 October 2004
- journal article
- research article
- Published by SAGE Publications in Journal of International Medical Research
- Vol. 32 (5), 465-483
- https://doi.org/10.1177/147323000403200503
Abstract
We examined the effects of β2-adrenergic receptor (β2-AR) agonists on the expression of co-stimulatory molecules on lipopoly-saccharide (LPS)-stimulated human peripheral blood mononuclear cells. The study found that β2-AR agonists inhibited the expression of intercellular adhesion molecule-1 (ICAM-1), CD40 and CD14 on monocytes, and that AR agonist activity was antagonized by the selective β2-AR antagonist, butoxamine. The selective β2-AR agonists salbutamol and terbutaline induced a similar co-stimulatory molecule expression pattern. The LPS-induced production of tumour necrosis factor-α was inhibited by AR agonists, and this was also antagonized by butoxamine, and mimicked by salbutamol and terbutaline. The AR agonists also inhibited T-cell proliferation through β2-AR stimulation. This study clearly demonstrated that endogenous catecholamines elicited immunosuppressive effects through β2-AR stimulation, possibly due to down-regulation of the expression of ICAM-1, CD40 and CD14 on monocytes. These results suggested that the sympathetic nervous system might regulate the T-helper cell balance via the peripheral end-effectors of the stress system.Keywords
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