Source:http://linkedlifedata.com/resource/pubmed/id/20042588
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2010-1-21
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pubmed:abstractText |
There is limited knowledge on the identity of primary CD4(+) T cell subsets selectively targeted by HIV-1 in vivo. In this study, we established a link between HIV permissiveness, phenotype/homing potential, and lineage commitment in primary CD4(+) T cells. CCR4(+)CCR6(+), CCR4(+)CCR6(-), CXCR3(+)CCR6(+), and CXCR3(+)CCR6(-) T cells expressed cytokines and transcription factors specific for Th17, Th2, Th1Th17, and Th1 lineages, respectively. CCR4(+)CCR6(+) and CXCR3(+)CCR6(+) T cells expressed the HIV coreceptors CCR5 and CXCR4 and were permissive to R5 and X4 HIV replication. CCR4(+)CCR6(-) T cells expressed CXCR4 but not CCR5 and were permissive to X4 HIV only. CXCR3(+)CCR6(-) T cells expressed CCR5 and CXCR4 but were relatively resistant to R5 and X4 HIV in vitro. Total CCR6(+) T cells compared with CCR6(-) T cells harbored higher levels of integrated HIV DNA in treatment-naive HIV-infected subjects. The frequency of total CCR6(+) T cells and those of CCR4(+)CCR6(+) and CXCR3(+)CCR6(+) T cells were diminished in chronically infected HIV-positive subjects, despite viral-suppressive therapy. A high-throughput analysis of cytokine profiles identified CXCR3(+)CCR6(+) T cells as a major source of TNF-alpha and CCL20 and demonstrated a decreased TNF-alpha/IL-10 ratio in CXCR3(+)CCR6(-) T cells. Finally, CCR4(+)CCR6(+) and CXCR3(+)CCR6(+) T cells exhibited gut- and lymph node-homing potential. Thus, we identified CCR4(+)CCR6(+) and CXCR3(+)CCR6(+) T cells as highly permissive to HIV replication, with potential to infiltrate and recruit more CCR6(+) T cells into anatomic sites of viral replication. It is necessary that new therapeutic strategies against HIV interfere with viral replication/persistence in discrete CCR6(+) T cell subsets.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Retroviral Agents,
http://linkedlifedata.com/resource/pubmed/chemical/CCR4 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/CCR6 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/CXCR3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/IL17A protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-17,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CCR4,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CCR6,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CXCR3
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1550-6606
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pubmed:author |
pubmed-author:AncutaPetronelaP,
pubmed-author:BoulasselMohamed-RachidMR,
pubmed-author:ChomontNicolasN,
pubmed-author:Diaz-GrifferoFelipeF,
pubmed-author:El-FarMohamedM,
pubmed-author:FonsecaSimoneS,
pubmed-author:GosselinAnnieA,
pubmed-author:MonteiroPatriciaP,
pubmed-author:RoutyJean-PierreJP,
pubmed-author:SaidElias AEA,
pubmed-author:SekalyRafick-PierreRP,
pubmed-author:WaclecheVanessaV
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pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
184
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1604-16
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pubmed:meshHeading |
pubmed-meshheading:20042588-Anti-Retroviral Agents,
pubmed-meshheading:20042588-CD4 Lymphocyte Count,
pubmed-meshheading:20042588-Disease Susceptibility,
pubmed-meshheading:20042588-HIV Infections,
pubmed-meshheading:20042588-HIV-1,
pubmed-meshheading:20042588-Immunity, Innate,
pubmed-meshheading:20042588-Immunophenotyping,
pubmed-meshheading:20042588-Interleukin-17,
pubmed-meshheading:20042588-Receptors, CCR4,
pubmed-meshheading:20042588-Receptors, CCR6,
pubmed-meshheading:20042588-Receptors, CXCR3,
pubmed-meshheading:20042588-T-Lymphocyte Subsets,
pubmed-meshheading:20042588-Th1 Cells,
pubmed-meshheading:20042588-Th2 Cells,
pubmed-meshheading:20042588-Virus Replication
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pubmed:year |
2010
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pubmed:articleTitle |
Peripheral blood CCR4+CCR6+ and CXCR3+CCR6+CD4+ T cells are highly permissive to HIV-1 infection.
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pubmed:affiliation |
Department of Microbiology and Immunology, Université de Montréal, Montreal, Quebec, Canada.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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