Expansion of a subset of CD14(high)CD16(neg)CCR2(low/neg) monocytes functionally similar to myeloid-derived suppressor cells during SIV and HIV infection

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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.authorGAMA, Lucio
dc.contributor.authorSHIRK, Erin N.
dc.contributor.authorRUSSELL, Julia N.
dc.contributor.authorCARVALHO, Karina I.
dc.contributor.authorLI, Ming
dc.contributor.authorQUEEN, Suzanne E.
dc.contributor.authorKALIL, Jorge
dc.contributor.authorZINK, M. Christine
dc.contributor.authorCLEMENTS, Janice E.
dc.contributor.authorKALLAS, Esper G.
dc.date.accessioned2013-07-30T14:41:37Z
dc.date.available2013-07-30T14:41:37Z
dc.date.issued2012
dc.description.abstractMonocytes have been categorized in three main subpopulations based on CD14 and CD16 surface expression. Classical monocytes express the CD14(++)CD16(-) CCR2(+) phenotype and migrate to inflammatory sites by quickly responding to CCL2 signaling. Here, we identified and characterized the expansion of a novel monocyte subset during HIV and SIV infection, which were undistinguishable from classical monocytes, based on CD14 and CD16 expression, but expressed significantly lower surface CCR2. Transcriptome analysis of sorted cells demonstrated that the CCR2(low/neg) cells are a distinct subpopulation and express lower levels of inflammatory cytokines and activation markers than their CCR2(high) counterparts. They exhibited impaired phagocytosis and greatly diminished chemotaxis in response to CCL2 and CCL7. In addition, these monocytes are refractory to SIV infection and suppress CD8(+) T cell proliferation in vitro. These cells express higher levels of STAT3 and NOS2, suggesting a phenotype similar to monocytic myeloid-derived cells, which suppress expansion of CD8(+) T cells in vivo. They may reflect an antiproliferative response against the extreme immune activation observed during HIV and SIV infections. In addition, they may suppress antiviral responses and thus, have a role in AIDS pathogenesis. Antiretroviral therapy in infected macaque and human subjects caused this population to decline, suggesting that this atypical phenotype is linked to viral replication. J. Leukoc. Biol. 91: 803-816; 2012.
dc.description.indexMEDLINE
dc.description.sponsorshipNational Institutes of Health (NIH) [MH070306, NS055648, MH085554]
dc.description.sponsorshipMinistry of Health [914/BRA/3014-UNESCO/Kallas]
dc.description.sponsorshipSao Paulo City Health Department [2004-0.168.922-7/Kallas]
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [04/15856-9]
dc.description.sponsorshipCoordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
dc.description.sponsorshipBrazilian Ministry of Education
dc.description.sponsorshipBrazilian Program for STD and AIDS
dc.identifier.citationJOURNAL OF LEUKOCYTE BIOLOGY, v.91, n.5, p.803-816, 2012
dc.identifier.doi10.1189/jlb.1111579
dc.identifier.issn0741-5400
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/392
dc.language.isoeng
dc.publisherFEDERATION AMER SOC EXP BIOL
dc.relation.ispartofJournal of Leukocyte Biology
dc.rightsrestrictedAccess
dc.rights.holderCopyright FEDERATION AMER SOC EXP BIOL
dc.subjectmacrophages
dc.subjectAIDS
dc.subject.othersimian immunodeficiency virus
dc.subject.otherperipheral-blood monocytes
dc.subject.otherchemokine receptor expression
dc.subject.othercentral-nervous-system
dc.subject.otherdendritic cells
dc.subject.othercc-chemokine
dc.subject.otherchemoattractant protein-1
dc.subject.othercerebrospinal-fluid
dc.subject.otherinflammatory sites
dc.subject.otherphenotypic changes
dc.subject.wosCell Biology
dc.subject.wosHematology
dc.subject.wosImmunology
dc.titleExpansion of a subset of CD14(high)CD16(neg)CCR2(low/neg) monocytes functionally similar to myeloid-derived suppressor cells during SIV and HIV infection
dc.typearticle
dc.type.categoryoriginal article
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.affiliation.countryEstados Unidos
hcfmusp.affiliation.countryisous
hcfmusp.author.externalSHIRK, Erin N.:Johns Hopkins Univ, Sch Med, Dept Mol & Comparat Pathobiol, Baltimore, MD 21287 USA
hcfmusp.author.externalRUSSELL, Julia N.:Johns Hopkins Univ, Sch Med, Dept Mol & Comparat Pathobiol, Baltimore, MD 21287 USA
hcfmusp.author.externalLI, Ming:Johns Hopkins Univ, Sch Med, Dept Mol & Comparat Pathobiol, Baltimore, MD 21287 USA
hcfmusp.author.externalQUEEN, Suzanne E.:Johns Hopkins Univ, Sch Med, Dept Mol & Comparat Pathobiol, Baltimore, MD 21287 USA
hcfmusp.author.externalZINK, M. Christine:Johns Hopkins Univ, Sch Med, Dept Mol & Comparat Pathobiol, Baltimore, MD 21287 USA
hcfmusp.author.externalCLEMENTS, Janice E.:Johns Hopkins Univ, Sch Med, Dept Mol & Comparat Pathobiol, Baltimore, MD 21287 USA
hcfmusp.citation.scopus52
hcfmusp.contributor.author-fmusphcLUCIO GAMA
hcfmusp.contributor.author-fmusphcKARINA INACIO LADISLAU DE CARVALHO SALMAZI
hcfmusp.contributor.author-fmusphcJORGE ELIAS KALIL FILHO
hcfmusp.contributor.author-fmusphcESPER GEORGES KALLAS
hcfmusp.description.beginpage803
hcfmusp.description.endpage816
hcfmusp.description.issue5
hcfmusp.description.volume91
hcfmusp.lim.ref2012
hcfmusp.origemWOS
hcfmusp.origem.pubmed22368280
hcfmusp.origem.scopus2-s2.0-84860898453
hcfmusp.origem.wosWOS:000303837200015
hcfmusp.publisher.cityBETHESDA
hcfmusp.publisher.countryUSA
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hcfmusp.remissive.sponsorshipCAPES
hcfmusp.remissive.sponsorshipFAPESP
hcfmusp.remissive.sponsorshipNIH
hcfmusp.remissive.sponsorshipMinistério da Saúde
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