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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0003320,
umls-concept:C0017262,
umls-concept:C0021756,
umls-concept:C0024264,
umls-concept:C0035820,
umls-concept:C0087111,
umls-concept:C0108747,
umls-concept:C0185117,
umls-concept:C0205160,
umls-concept:C0205217,
umls-concept:C0205263,
umls-concept:C1367475,
umls-concept:C1515655,
umls-concept:C1752435,
umls-concept:C2911684
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pubmed:issue |
13
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pubmed:dateCreated |
1989-7-27
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pubmed:abstractText |
The phenotype and function of lymphocytes from cancer patients treated with repetitive weekly cycles of continuous i.v. infusions of recombinant interleukin 2 (IL-2) were examined. Peripheral blood lymphocytes (PBL) obtained after IL-2 therapy showed an increased percentage of cells bearing the CD16 and leu19 markers which are associated with natural killer cells. These PBL mediated significantly increased levels of IL-2-dependent lymphokine-activated killer (LAK) activity against the Daudi cell line. Depletion of CD16+ cells from PBL obtained after in vivo IL-2 caused only slight inhibition of their LAK activity or their proliferative response to IL-2 in vitro. This indicates that CD16+ cells are involved but play only a minor role in these responses. In contrast, depletion of leu19+ cells, from PBL activated in vivo with IL-2, virtually abrogated their LAK activity and their proliferative response to IL-2. Two-color flow cytometry studies showed that a leu19+/CD16- population was expanded by in vivo IL-2 therapy and was responsible for the majority of LAK activity by in vivo-activated PBL. Moreover, this CD16- population showed an increased density of leu19 and CD2 (E rosette receptor) antigens when compared to the resting PBL obtained prior to IL-2 treatment. These data show that the predominant population mediating in vitro LAK activity, induced by in vivo IL-2 therapy, consists of activated natural killer cells with a high density of leu19 and CD2 antigens but negative for the CD16 antigen.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD2,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD56,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation...,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Fc,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, IgG,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Immunologic,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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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 |
49
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3680-8
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:2471587-Antigens, CD2,
pubmed-meshheading:2471587-Antigens, CD56,
pubmed-meshheading:2471587-Antigens, Differentiation,
pubmed-meshheading:2471587-Antigens, Differentiation, T-Lymphocyte,
pubmed-meshheading:2471587-Cell Separation,
pubmed-meshheading:2471587-Cytotoxicity, Immunologic,
pubmed-meshheading:2471587-Flow Cytometry,
pubmed-meshheading:2471587-Humans,
pubmed-meshheading:2471587-Immunity, Cellular,
pubmed-meshheading:2471587-Interleukin-2,
pubmed-meshheading:2471587-Killer Cells, Natural,
pubmed-meshheading:2471587-Lymphocyte Activation,
pubmed-meshheading:2471587-Lymphocytes,
pubmed-meshheading:2471587-Receptors, Fc,
pubmed-meshheading:2471587-Receptors, IgG,
pubmed-meshheading:2471587-Receptors, Immunologic,
pubmed-meshheading:2471587-Recombinant Proteins
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pubmed:year |
1989
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pubmed:articleTitle |
Lymphokine-activated killer activity induced by in vivo interleukin 2 therapy: predominant role for lymphocytes with increased expression of CD2 and leu19 antigens but negative expression of CD16 antigens.
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pubmed:affiliation |
Department of Human Oncology, University of Wisconsin, Madison.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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