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- Title
Beta2-adrenergic receptor signaling in CD4<sup>+</sup> Foxp3<sup>+</sup> regulatory T cells enhances their suppressive function in a PKA-dependent manner.
- Authors
Guereschi, Marcia G.; Araujo, Leandro P.; Maricato, Juliana T.; Takenaka, Maisa C.; Nascimento, Vanessa M.; Vivanco, Bruno C.; Reis, Vanessa O.; Keller, Alexandre C.; Brum, Patrícia C.; Basso, Alexandre S.
- Abstract
Beta2-adrenergic receptor ( B2 AR) signaling is known to impair Th1-cell differentiation and function in a c AMP-dependent way, leading to inhibition of cell proliferation and decreased production of IL-2 and IFN-γ. CD4+ Foxp3+ Treg cells play a key role in the regulation of immune responses and are essential for maintenance of self-tolerance. Nevertheless, very little is known about adrenergic receptor expression in Treg cells or the influence of noradrenaline on their function. Here we show that Foxp3+ Treg cells express functional B2 AR. B2 AR activation in Treg cells leads to increased intracellular c AMP levels and to protein kinase A ( PKA)-dependent CREB phosphorylation. We also found that signaling via B2 AR enhances the in vitro suppressive activity of Treg cells. B2 AR-mediated increase in Treg-cell suppressive function was associated with decreased IL-2 m RNA levels in responder CD4+ T cells and improved Treg-cell-induced conversion of CD4+ Foxp3− cells into Foxp3+ induced Treg cells. Moreover, B2 AR signaling increased CTLA-4 expression in Treg cells in a PKA-dependent way. Finally, we found that PKA inhibition totally prevented the B2 AR-mediated increase in Treg-cell suppressive function. Our data suggest that sympathetic fibers are able to regulate Treg-cell suppressive activity in a positive manner through B2 AR signaling.
- Publication
European Journal of Immunology, 2013, Vol 43, Issue 4, p1001
- ISSN
0014-2980
- Publication type
Article
- DOI
10.1002/eji.201243005