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J Neuroimmunol. 2004 Oct;155(1-2):143-9.

Post-receptorial mechanisms underlie functional disregulation of beta2-adrenergic receptors in lymphocytes from Multiple Sclerosis patients.

Author information

1
Department of Neurologic and Psychiatric Sciences, University of Bari, I-70124 Bari, Italy. mgiorelli@libero.it

Abstract

Increased density of beta2-adrenergic receptors has been demonstrated on peripheral blood mononuclear cells (PBMCs) from Multiple Sclerosis (MS) patients. In this study we found that isoproterenol reduces T-cell proliferation and IFNgamma secretion in PBMCs cultures from healthy controls and IFNbeta-treated but not untreated MS patients. Reduced expression levels of G protein coupled receptor kinase (GRK)2/3 (p < 0.05) and increased isoproterenol-induced cAMP accumulation (p < 0.0001) were found in PBMCs from all MS patients. Dibutyryl cAMP reduced the proliferation of PBMCs from all subgroups but in a slighter manner in untreated MS patients. We conclude that signalling through beta2-adrenergic receptors is chronically up-regulated but functionally uncoupled to immunoregulatory functions of lymphocytes from MS patients. Disregulation downstream the cAMP-associated signalling may underlie such a phenomenon.

PMID:
15342205
DOI:
10.1016/j.jneuroim.2004.05.013
[Indexed for MEDLINE]

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