Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/31037
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dc.contributor.authorSandri, Silvana
dc.contributor.authorHatanaka, Elaine
dc.contributor.authorFranco, Andressa G.
dc.contributor.authorPedrosa, Alziana M. C.
dc.contributor.authorMonteiro, Hugo P. [UNIFESP]
dc.contributor.authorCampa, Ana
dc.date.accessioned2016-01-24T13:51:53Z-
dc.date.available2016-01-24T13:51:53Z-
dc.date.issued2008-11-16
dc.identifierhttp://dx.doi.org/10.1016/j.imlet.2008.07.013
dc.identifier.citationImmunology Letters. Amsterdam: Elsevier B.V., v. 121, n. 1, p. 22-26, 2008.
dc.identifier.issn0165-2478
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/31037-
dc.description.abstractAlthough the serum levels of SAA had been reported to be upregulated during inflammatory/infectious process, the role of this acute-phase protein has not been completely elucidated. in previous studies, we demonstrated that SAA stimulated the production of TNF-alpha, IL-1 beta, IL-8, NO, and ROS by neutrophils and/or mononuclear cells. Herein we demonstrate that SAA induces the expression and release of CCL20 from Cultured human blood mononuclear cells. We also focus on the signaling pathways triggered by SAA. in THP-1 cells SAA promotes phosphorylation of p38 and ERK1/2. Furthermore, the addition of SB203580 (p38 inhibitor) and PD98059 (ERK 1/2 inhibitor) inhibits the expression and release of CCL20 in mononuclear cells treated with SAA. Our results point to SAA as an important link of innate to adaptive immunity, once it might act on the recruitment of mononuclear cells. (C) 2008 Elsevier B.V. All rights reserved.en
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.format.extent22-26
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofImmunology Letters
dc.rightsAcesso restrito
dc.subjectCCL20en
dc.subjectMononuclear cells and serum amyloid A (SAA)en
dc.titleSerum amyloid A induces CCL20 secretion in mononuclear cells through MAPK (p38 and ERK1/2) signaling pathwaysen
dc.typeArtigo
dc.rights.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniv Cruzeiro
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.description.affiliationUniv São Paulo, Fac Ciencias Farmaceut, Dept Anal Clin & Toxicol, BR-05508900 São Paulo, Brazil
dc.description.affiliationUniv São Paulo, Inst Ciencias Biomed, Dept Fisiol & Biofis, BR-05508900 São Paulo, Brazil
dc.description.affiliationUniv Cruzeiro, Area Ciencias Biol & Saude, São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Dept Bioquim, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Bioquim, São Paulo, Brazil
dc.identifier.doi10.1016/j.imlet.2008.07.013
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000261280600004
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