| Autor: |
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. |
| Zdroj: |
European Journal of Immunology; Apr2013, Vol. 43 Issue 4, p1001-1012, 12p |
| Abstrakt: |
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. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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