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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
21
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pubmed:dateCreated |
1995-12-6
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pubmed:abstractText |
Interleukin 15 (IL-15) is a novel cytokine that shares no homology with IL-2, but it requires the use of beta and gamma chains of the IL-2 receptor complex for binding and signaling. In vitro studies have shown induction of CTL and lymphokine-activated killer (LAK) cell activity in peripheral blood mononuclear cells (PBMCs) from normal donors by IL-15 against known tumor targets. The present study attempts to define the role of IL-15 in generating LAK activity from melanoma patient lymphocytes. PBMCs of patients newly diagnosed with metastatic melanoma were incubated with different doses of recombinant human IL-15 and tested against autologous tumor cells, LAK sensitive cell lines (i.e., FMEX and Daudi), as well as the natural killer-sensitive cell line K562, in a 15-h 51Cr release assay. The effect of IL-15 was found to be both time and dose dependent, with peak activity detected after 2 or 3 days of culture with 100 ng/ml of this cytokine. LAK and not CTL activity in patient PBMCs was detected by the inability of mAbs against CD4, CD8, and MHC class I to effectively block lysis of autologous tumor and FMEX melanoma cells. In addition, interaction via the CD18 adhesion molecule was shown to be critical in IL-15-induced LAK-mediated lysis of autologous tumor cells. Finally, incubation of patient PBMCs with IL-15 for 6 h resulted in the up-regulation of perforin mRNA transcription. These findings suggest that LAK activity can be generated from melanoma patient PBMCs in the presence of IL-15 to lyse autologous tumor cells in a non-MHC-restricted manner. This new cytokine may play an important role in antitumor immunity with a possible use for cancer immunotherapy.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0008-5472
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
55
|
pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4988-94
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:7585540-Antigens, CD18,
pubmed-meshheading:7585540-Biopsy,
pubmed-meshheading:7585540-Humans,
pubmed-meshheading:7585540-Immunotherapy,
pubmed-meshheading:7585540-Interleukin-15,
pubmed-meshheading:7585540-Interleukins,
pubmed-meshheading:7585540-Killer Cells, Lymphokine-Activated,
pubmed-meshheading:7585540-Lymphocyte Activation,
pubmed-meshheading:7585540-Lymphocytes,
pubmed-meshheading:7585540-Melanoma,
pubmed-meshheading:7585540-Membrane Glycoproteins,
pubmed-meshheading:7585540-Sensitivity and Specificity,
pubmed-meshheading:7585540-Stimulation, Chemical,
pubmed-meshheading:7585540-Transcription, Genetic
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pubmed:year |
1995
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pubmed:articleTitle |
Interleukin 15 induction of lymphokine-activated killer cell function against autologous tumor cells in melanoma patient lymphocytes by a CD18-dependent, perforin-related mechanism.
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pubmed:affiliation |
Department of Biochemistry, University of South Florida, College of Medicine, Tampa, USA.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.
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