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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0039194,
umls-concept:C0086418,
umls-concept:C0254610,
umls-concept:C0439097,
umls-concept:C0871261,
umls-concept:C1291775,
umls-concept:C1547348,
umls-concept:C1552644,
umls-concept:C1704632,
umls-concept:C1705241,
umls-concept:C1706817,
umls-concept:C1823153,
umls-concept:C1947976,
umls-concept:C2349975,
umls-concept:C2349976,
umls-concept:C2911692
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pubmed:issue |
9
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pubmed:dateCreated |
1998-5-21
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pubmed:abstractText |
Human gamma delta T cells have the ability to rapidly expand and produce IFN-gamma in response to nonpeptide Ags of microbial pathogens, in particular a class of compounds known as the prenyl phosphates. We investigated the ability of IL-15, a T cell growth factor, to modulate prenyl phosphate-induced gamma delta T cell proliferation and cytokine production. IL-15 significantly enhanced the expansion of gamma delta T cells in the peripheral blood after stimulation in vitro with isopentenyl pyrophosphate. Moreover, using gamma delta T cell clones, we determined that IL-15-induced T cell proliferation was dependent on the IL-2R beta chain but not the IL-2R alpha chain. We therefore studied the IL-15R alpha chain expression in human gamma delta T cells in the presence or absence of nonpeptide Ags. We found IL-15R alpha mRNA expression in IL-15-stimulated and Ag-stimulated human gamma delta T cells but not in resting gamma delta T cells. Although IL-15 itself had little effect on the production of IFN-gamma, IL-15 plus IL-12 acted synergistically to augment IFN-gamma production by gamma delta T cells. Moreover, we showed that this increase in IFN-gamma could be explained by the dual activation of STAT1 and STAT4 by IL-15 and IL-12, respectively. Taken together, these results suggest that IL-15 may contribute to activation of human gamma delta T cells in the immune response to microbial pathogens.
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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, Bacterial,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Diphosphates,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-15,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell...
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
160
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4322-9
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:9574535-Antigens, Bacterial,
pubmed-meshheading:9574535-Cell Division,
pubmed-meshheading:9574535-Clone Cells,
pubmed-meshheading:9574535-Cytokines,
pubmed-meshheading:9574535-Diphosphates,
pubmed-meshheading:9574535-Humans,
pubmed-meshheading:9574535-Interleukin-15,
pubmed-meshheading:9574535-Lymphocyte Activation,
pubmed-meshheading:9574535-Receptors, Antigen, T-Cell, gamma-delta,
pubmed-meshheading:9574535-T-Lymphocyte Subsets
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pubmed:year |
1998
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pubmed:articleTitle |
IL-15 enhances the response of human gamma delta T cells to nonpeptide [correction of nonpetide] microbial antigens.
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pubmed:affiliation |
Division of Dermatology, UCLA School of Medicine, Los Angeles, CA 90095, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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