Polyfunctional natural killer cells with a low activation profile in response to Toll-like receptor 3 activation in HIV-1-exposed seronegative subjects

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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorLIMA, Josenilson F.
dc.contributor.authorOLIVEIRA, Luanda M. S.
dc.contributor.authorPEREIRA, Natalli Z.
dc.contributor.authorDUARTE, Alberto J. S.
dc.contributor.authorSATO, Maria N.
dc.date.accessioned2017-06-09T15:37:40Z
dc.date.available2017-06-09T15:37:40Z
dc.date.issued2017
dc.description.abstractNatural killer (NK) cells are the main mediator of the cytotoxic response in innate immunity and may be involved in resistance to HIV-1 infection in exposed seronegative (ESN) individuals. Toll-like receptor (TLR) signalling is crucial for NK cell activation. Here, we investigated the polyfunctional NK cell response to TLR3 activation in serodiscordant couples. ESN subjects showed increased IFN-gamma. and CD107a expression in both NK subsets, CD56(bright) and CD56(dim) cells, in response to stimulation with a TLR3 agonist, while expression was impaired in the HIV-1-infected partners. TLR3-induced expression of IFN-gamma, TNF and CD107a by polyfunctional CD56bright NK cells was more pronounced in ESN individuals than that in healthy controls. Activated NK cells, as determined by CD38 expression, were increased only in the HIV-1-infected partners, with reduced IFN-gamma. and CD107a expression. Moreover, CD38(+) NK cells of the HIV-1-infected partners were associated with increased expression of inhibitory molecules, such as NKG2A, PD- 1 and Tim-3, while NK cells from ESN subjects showed decreased NKG2A expression. Altogether, these findings indicate that NK cells of ESN individuals were highly responsive to TLR3 activation and had a polyfunctional NK cell phenotype, while the impaired TLR3 response in HIV-1-infected partners was associated with an inhibitory/ exhaustion NK cell phenotype.
dc.description.indexMEDLINE
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo [2015/00263-7]
dc.description.sponsorshipLaboratorio de Investigacao Medica, Unidade 56 do Hospital das Clinicas da Faculdade de Medicina de Sao Paulo
dc.identifier.citationSCIENTIFIC REPORTS, v.7, article ID 524, 9p, 2017
dc.identifier.doi10.1038/s41598-017-00637-3
dc.identifier.issn2045-2322
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/20182
dc.language.isoeng
dc.publisherNATURE PUBLISHING GROUP
dc.relation.ispartofScientific Reports
dc.rightsopenAccess
dc.rights.holderCopyright NATURE PUBLISHING GROUP
dc.subject.otherexposed uninfected individuals
dc.subject.otherhiv-1 infection
dc.subject.othert-cells
dc.subject.otherintegrin alpha(4)beta(7)
dc.subject.otherantiretroviral therapy
dc.subject.otherimmune activation
dc.subject.othernk cells
dc.subject.otherexpression
dc.subject.otherresistance
dc.subject.otherlevel
dc.subject.wosMultidisciplinary Sciences
dc.titlePolyfunctional natural killer cells with a low activation profile in response to Toll-like receptor 3 activation in HIV-1-exposed seronegative subjects
dc.typearticle
dc.type.categoryoriginal article
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.citation.scopus21
hcfmusp.contributor.author-fmusphcJOSENILSON FEITOSA DE LIMA
hcfmusp.contributor.author-fmusphcLUANDA MARA DA SILVA OLIVEIRA
hcfmusp.contributor.author-fmusphcNATALLI ZANETE PEREIRA
hcfmusp.contributor.author-fmusphcALBERTO JOSE DA SILVA DUARTE
hcfmusp.contributor.author-fmusphcMARIA NOTOMI SATO
hcfmusp.description.articlenumber524
hcfmusp.description.volume7
hcfmusp.origemWOS
hcfmusp.origem.pubmed28373665
hcfmusp.origem.scopus2-s2.0-85017118586
hcfmusp.origem.wosWOS:000398134800001
hcfmusp.publisher.cityLONDON
hcfmusp.publisher.countryENGLAND
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