Norepinephrine controls effector t cell differentiation through beta 2-adrenergic receptor-mediated inhibition of nf-kappa b and ap-1 in dendritic cells

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dc.contributor.authorTakenaka, Maisa Carla [UNIFESP]
dc.contributor.authorAraujo, Leandro Pires [UNIFESP]
dc.contributor.authorMaricato, Juliana Terzi [UNIFESP]
dc.contributor.authorNascimento, Vanessa de Mendonça [UNIFESP]
dc.contributor.authorGuereschi, Marcia Grando [UNIFESP]
dc.contributor.authorRezende, Rafael Machado
dc.contributor.authorQuintana, Francisco J.
dc.contributor.authorBasso, Alexandre Salgado [UNIFESP]
dc.date.accessioned2019-01-21T10:29:20Z
dc.date.available2019-01-21T10:29:20Z
dc.date.issued2016
dc.description.abstractDespite 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 proliferationen
dc.description.abstracthowever, 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.en
dc.description.affiliationDepartamento de Microbiologia, Imunologia, e Parasitologia, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo 04023-062, Brazil
dc.description.affiliationAnn Romney Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115
dc.description.affiliationUnifespDepartamento de Microbiologia, Imunologia, e Parasitologia, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo 04023-062, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)
dc.description.sponsorshipIDFAPESP: 2008/58564-9
dc.description.sponsorshipIDCNPq: 475000/2010-2
dc.description.sponsorshipIDCNPq: 246252/2012-0
dc.format.extent637-644
dc.identifierhttps://doi.org/10.4049/jimmunol.1501206
dc.identifier.citationJournal Of Immunology. Bethesda, v. 196, n. 2, p. 637-644, 2016.
dc.identifier.doi10.4049/jimmunol.1501206
dc.identifier.issn0022-1767
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/49182
dc.identifier.wosWOS:000368072100020
dc.language.isoeng
dc.publisherAmer Assoc Immunologists
dc.relation.ispartofJournal Of Immunology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectElement-Binding Proteinen
dc.subjectBone-Marrowen
dc.subjectBeta(2)-Adrenergic Receptoren
dc.subjectCytokine Productionen
dc.subjectMolecular-Mechanismsen
dc.subjectInnate Immunityen
dc.subjectKinaseen
dc.subjectBetaen
dc.subjectActivationen
dc.subjectAgonistsen
dc.titleNorepinephrine controls effector t cell differentiation through beta 2-adrenergic receptor-mediated inhibition of nf-kappa b and ap-1 in dendritic cellsen
dc.typeinfo:eu-repo/semantics/article
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