Please use this identifier to cite or link to this item: http://repositorio.unifesp.br/handle/11600/49182
Title: Norepinephrine controls effector t cell differentiation through beta 2-adrenergic receptor-mediated inhibition of nf-kappa b and ap-1 in dendritic cells
Authors: Takenaka, Maisa Carla [UNIFESP]
Araujo, Leandro Pires [UNIFESP]
Maricato, Juliana Terzi [UNIFESP]
Nascimento, Vanessa de Mendonça [UNIFESP]
Guereschi, Marcia Grando [UNIFESP]
Rezende, Rafael Machado
Quintana, Francisco J.
Basso, Alexandre Salgado [UNIFESP]
Keywords: Element-Binding Protein
Bone-Marrow
Beta(2)-Adrenergic Receptor
Cytokine Production
Molecular-Mechanisms
Innate Immunity
Kinase
Beta
Activation
Agonists
Issue Date: 2016
Publisher: Amer Assoc Immunologists
Citation: Journal Of Immunology. Bethesda, v. 196, n. 2, p. 637-644, 2016.
Abstract: Despite accumulating evidence indicating that neurotransmitters released by the sympathetic nervous system can modulate the activity of innate immune cells, we still know very little about how norepinephrine impacts signaling pathways in dendritic cells (DC) and the consequence of that in DC-driven T cell differentiation. In this article, we demonstrate that beta(2)-adrenergic receptor (beta(2)AR) activation in LPS-stimulated DC does not impair their ability to promote T cell proliferation
however, it diminishes IL-12p70 secretion, leading to a shift in the IL-12p70/IL-23 ratio. Although beta(2)AR stimulation in DC induces protein kinase A-dependent cAMP-responsive element-binding protein phosphorylation, the effect of changing the profile of cytokines produced upon LPS challenge occurs in a protein kinase A-independent manner and, rather, is associated with inhibition of the NF-kappa B and AP-1 signaling pathways. Moreover, as a consequence of the inverted IL-12p70/IL-23 ratio following beta(2)AR stimulation, LPS-stimulated DC promoted the generation of CD4(+) T cells that, upon TCR engagement, produced lower amounts of IFN-gamma and higher levels of IL-17. These findings provide new insights into molecular and cellular mechanisms by which beta(2)AR stimulation in murine DC can influence the generation of adaptive immune responses and may explain some aspects of how sympathetic nervous system activity can modulate immune function.
URI: http://repositorio.unifesp.br/handle/11600/49182
ISSN: 0022-1767
Other Identifiers: https://doi.org/10.4049/jimmunol.1501206
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