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• W1984470860 abstract "The sympathetic nervous system (SNS) is able to modulate immune functions via adrenoceptor-dependent mechanisms. Activation of β2-adrenergic receptors (AR) on CD4+ T lymphocytes has been shown to inhibit Th1-cytokine production and cell proliferation. Here, we investigated the role of the calcium/calmodulin-dependent protein phosphatase calcineurin (CaN), a key element of the T cell receptor (TCR)-signaling pathway, in β2-AR-mediated suppression of T cell function. Purified rat splenic CD4+ T cells were stimulated with anti-CD3/anti-CD28 in presence or absence of the β2-AR agonist terbutaline (TERB). Treatment with TERB induced a dose-dependent inhibition of cellular CaN activity, along with a reduction in IL-2 and IFN-γ production, and T cell proliferation. Co-administration of the β-AR antagonist nadolol abolished these effects. Blockade of the cAMP-dependent protein kinase A (PKA) with the inhibitor H-89 completely prevented TERB-induced CaN inhibition. However, a receptor-independent rise in the second messenger cAMP was not sufficient to suppress CaN activity. Disruption of the interaction between PKA and A-kinase anchoring protein (AKAP) by the inhibitor peptide St-Ht31 fully blocked TERB-induced CaN inhibition, demonstrating that PKA–AKAP interaction is essential for the β2-AR-mediated CaN inhibition. Taken together, this study provides evidence for a link between the β2-AR and TCR signaling pathways since expression of IL-2 and IFN-γ in activated T cells largely depends on dephosphorylation of the transcription factor NFAT by CaN, and identifies a novel intracellular mechanism that can lead to downregulation of T cell function after SNS activation." @default.
• W1984470860 created "2016-06-24" @default.
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• W1984470860 date "2011-01-01" @default.
• W1984470860 modified "2023-09-27" @default.
• W1984470860 title "Stimulation of β2-adrenergic receptors inhibits calcineurin activity in CD4+ T cells via PKA–AKAP interaction" @default.
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• W1984470860 doi "https://doi.org/10.1016/j.bbi.2010.07.248" @default.
• W1984470860 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20674738" @default.
• W1984470860 hasPublicationYear "2011" @default.
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