Source:http://linkedlifedata.com/resource/pubmed/id/10438976
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
1999-9-9
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pubmed:abstractText |
Memory T cells that home to inflamed tissues typically express the beta-chemokine receptor CCR5 and exhibit a Th1 cytokine profile. The migration of these cells into the genital tract following antigenic exposure has particular relevance to acquisition of HIV-1 infection, because CCR5 functions as the coreceptor for most sexually transmitted HIV-1 strains. We recently established methodology to purify and culture mononuclear cells from the female reproductive tract, and here we analyzed the phenotype, CCR5 expression, and cytokine production of cervicovaginal T cells in up to 16 donors. The proportion of mucosal T cells expressing CCR5 was markedly expanded as compared with peripheral blood (mean 88% vs 24% in 13 donors), but the receptor density on individual CCR5+ T cells was only slightly increased (mean 5837 vs 4191 MEPE (molecules of equivalent PE) units in 6 of 7 donors). Intracellular costaining for IL-2, IFN-gamma, IL-4, and IL-5 revealed a Th1-type pattern in cervical T cells, with significantly higher percentages of IL-2- and IFN-gamma-producing T cells in the mucosa than in blood (mean 67% vs 29%). Coexpression of surface CCR5 with intracellular IL-2 and IFN-gamma was observed only among T cells in the mucosa, but not among those in circulation. Thus, we postulate that T cell homing to the genital mucosa leads to differentiation into the combined CCR5+ Th1 phenotype. Moreover, the predominance of CCR5+ Th1-type T cells in normal cervical mucosa provides targets accessible for the efficient transmission of macrophage-tropic HIV-1 variants in women following sexual exposure.
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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/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD45,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation...,
http://linkedlifedata.com/resource/pubmed/chemical/CD69 antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Lectins, C-Type,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell...,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CCR5,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Lymphocyte Homing
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
163
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2306-13
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:10438976-Antigens, CD,
pubmed-meshheading:10438976-Antigens, CD45,
pubmed-meshheading:10438976-Antigens, Differentiation, T-Lymphocyte,
pubmed-meshheading:10438976-Cell Separation,
pubmed-meshheading:10438976-Cervix Uteri,
pubmed-meshheading:10438976-Female,
pubmed-meshheading:10438976-Humans,
pubmed-meshheading:10438976-Immunophenotyping,
pubmed-meshheading:10438976-Interferon-gamma,
pubmed-meshheading:10438976-Interleukin-2,
pubmed-meshheading:10438976-Lectins, C-Type,
pubmed-meshheading:10438976-Mucous Membrane,
pubmed-meshheading:10438976-Receptors, Antigen, T-Cell, alpha-beta,
pubmed-meshheading:10438976-Receptors, CCR5,
pubmed-meshheading:10438976-Receptors, Lymphocyte Homing,
pubmed-meshheading:10438976-T-Lymphocyte Subsets,
pubmed-meshheading:10438976-Th1 Cells,
pubmed-meshheading:10438976-Vagina
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pubmed:year |
1999
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pubmed:articleTitle |
Coexpression of CCR5 and IL-2 in human genital but not blood T cells: implications for the ontogeny of the CCR5+ Th1 phenotype.
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pubmed:affiliation |
Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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