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Activated T helper 1 and T helper 2 cells differentially express the beta-2-adrenergic receptor: a mechanism for selective modulation of T helper 1 cell cytokine production.

Authors
  • Ramer-Quinn, D S
  • Baker, R A
  • Sanders, V M
Type
Published Article
Journal
Journal of immunology (Baltimore, Md. : 1950)
Publication Date
Nov 15, 1997
Volume
159
Issue
10
Pages
4857–4867
Identifiers
PMID: 9366411
Source
Medline
License
Unknown

Abstract

We recently reported that resting clones of murine Th1 cells, but not resting Th2 cells, expressed a detectable level of the beta-2-adrenergic receptor (beta 2AR). In the present study, we proposed that the level of beta 2AR expression on anti-CD3 mAb-activated CD4+ effector Th cells may differ from the level on resting cells, and that a change in receptor expression may alter the functional responsiveness of these cells to either the beta 2AR-selective ligand terbutaline or the sympathetic neurotransmitter norepinephrine. Following anti-CD3 activation, the beta 2AR was expressed on Th1 cells, but not Th2 cells. The number of binding sites on Th1 cells was maintained, with no change in affinity, over a 24-h activation period. When Th clones were exposed to terbutaline following anti-CD3 activation, Th1 cell, but not Th2 cell, cytokine production was modulated. IL-2 production by Th1 cells was decreased, while IFN-gamma production was not significantly altered. The decrease in IL-2 production was concentration dependent and was blocked by an antagonist. In comparison with control supernatants, the lower level of IL-2 present in terbutaline-exposed culture supernatants supported the proliferation of an IL-2-dependent Th1 clone to a lesser degree. Additionally, norepinephrine down-modulates IL-2, but not IFN-gamma, production by binding specifically to the beta-adrenergic receptor. Thus, a detectable level of the beta 2AR is expressed on activated Th1 cells, but not activated Th2 cells, thereby providing a mechanism by which IL-2 production is preferentially modulated by an endogenous and therapeutic ligand following Th1 cell activation.

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