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dc.creatorStojić-Vukanić, Zorica
dc.creatorNacka-Aleksić, Mirjana
dc.creatorBufan, Biljana
dc.creatorPilipović, Ivan
dc.creatorArsenović-Ranin, Nevena
dc.creatorĐikić, Jasmina
dc.creatorKosec, Duško
dc.creatorLeposavić, Gordana
dc.date.accessioned2021-02-18T10:45:21Z
dc.date.available2021-02-18T10:45:21Z
dc.date.issued2015
dc.identifier.issn1567-5769
dc.identifier.urihttp://intor.torlakinstitut.com/handle/123456789/442
dc.description.abstractThis study was undertaken considering that, despite the broad use of the unopposed estrogen replacement therapy in elderly women, data on estrogen influence on the functional capacity of dendritic cells (DCs), and consequently immune response are limited. We examined the influence of 17 beta-estradiol on phenotype, cytokine secretory profile, and allostimulatory and polarizing capacity of splenic (OX62+) conventional DCs from 26-month-old (aged) Albino Oxford rats matured in vitro in the presence of LPS, a TLR4 agonist, and R848, a TLR7/8 agonist In the presence of 17 beta-estradiol, DCs from aged rats exhibited an impaired ability to mature upon stimulation with LPS, as shown by the lower surface density of MHC II and costimulatory CD80 and CD86 molecules. 17 beta-Estradiol alone enhanced CD40 expression in OX62+ DCs without affecting the expression of other costimulatory molecules, thereby confirming that the expression of this molecule is regulated independently from the regulation of other costimulatory molecules. However, although R848 upregulated the expression of MHC II and CD80 and CD40 costimulatory molecules on DCs, 17 beta-estradiol diminished the effect of this TLR agonist only on MHC II expression. In conjunction, the previous findings suggest that LPS and R848 elicit changes in the expression of costimulatory molecules via triggering differential intracellular signaling pathways. Furthermore, 17 beta-estradiol diminished the stimulatory influence of both LPS- and R848-matured OX62+ DCs on allogeneic CD4+ T lymphocyte proliferation in a mixed lymphocyte reaction (MLR). Moreover, as shown in MLR, the exposure to 17 beta-estradiol during LPS- and R848-induced maturation diminished Th1- and enhanced Th17-driving capacity and reduced Th1-driving capacity of OX62+ DCs, respectively. This suggests that LPS and R848 affect not only the surface phenotype, but also functional characteristics of OX62+ DCs triggering distinct intracellular signaling pathways. Collectively, the findings indicate that estrogen directly acting on OX62+ DCs, may affect CD4+ lymphocyte-dependent immune response in aged female rats. (C) 2014 Elsevier B.V. All rights reserved.en
dc.publisherElsevier, Amsterdam
dc.relationinfo:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/175050/RS//
dc.rightsrestrictedAccess
dc.sourceInternational Immunopharmacology
dc.subjectAgingen
dc.subject17 beta-Estradiolen
dc.subjectConventional dendritic cellsen
dc.subjectTh polarizationen
dc.subjectCytokinesen
dc.subjectRaten
dc.title17 beta-Estradiol influences in vitro response of aged rat splenic conventional dendritic cells to TLR4 and TLR7/8 agonists in an agonist specific manneren
dc.typearticle
dc.rights.licenseARR
dc.citation.epage35
dc.citation.issue1
dc.citation.other24(1): 24-35
dc.citation.rankM22
dc.citation.spage24
dc.citation.volume24
dc.identifier.doi10.1016/j.intimp.2014.11.008
dc.identifier.pmid25479725
dc.identifier.scopus2-s2.0-84911927954
dc.identifier.wos000348621900004
dc.type.versionpublishedVersion


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