rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
10
|
pubmed:dateCreated |
2005-11-3
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pubmed:abstractText |
To study natural killer (NK) cell-mediated antileukemic activity in chronic myelogenous leukemia (CML), we investigated the ability of HLA-matched and mismatched CD56(+) cells to inhibit granulocyte macrophage-colony-forming unit (CFU-GM) formation by leukemic CD34(+) cells. In 14 HLA-identical donor-recipient pairs, donor CD56(+) cells inhibited CML CFU-GM comparably to effectors from 14 HLA-mismatched unrelated individuals (mean inhibition 42% +/- 9% vs 39.5% +/- 7% at a 10:1 effector-to-target (E/T) ratio), suggesting that killer inhibitory receptor (KIR) incompatibility was not essential for an antileukemic effect. Both CD56(+)CD3(-) (natural killer [NK]) and CD56(+)CD3(+)(NK-T) cells inhibited CFU-GM growth of CML but not normal CD34(+) cells. A mechanism for this leukemia-specific cytotoxicity was suggested by the abnormal overexpression of major histocompatibility class I chain-related gene A or gene B (MICA/B) on CML CD34 cells and their ability to bind the NK activation ligand NKG2D. However, in vivo, CML cells may avoid NK-cell-mediated immune destruction by immune escape, shedding MICA into the plasma, thereby down-regulating NKG2D on CML CD56(+) cells.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/16046526-10359807,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16046526-10381530,
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
AIM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/HLA Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class I,
http://linkedlifedata.com/resource/pubmed/chemical/KLRK1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/MHC class I-related chain A,
http://linkedlifedata.com/resource/pubmed/chemical/MICB antigen,
http://linkedlifedata.com/resource/pubmed/chemical/NK Cell Lectin-Like Receptor...,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Immunologic,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Natural Killer Cell
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
|
pubmed:issn |
0006-4971
|
pubmed:author |
pubmed-author:BarrettA JohnAJ,
pubmed-author:FerroneSoldanoS,
pubmed-author:FujiwaraHiroshiH,
pubmed-author:HenselNancyN,
pubmed-author:LauMichelleM,
pubmed-author:LiJonmingJ,
pubmed-author:MelenhorstJosJ,
pubmed-author:ProvenzanoMaurizioM,
pubmed-author:RezvaniKatayounK,
pubmed-author:SconocchiaGiuseppeG,
pubmed-author:WongsenaWachananW
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
106
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
3666-72
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:16046526-Adult,
pubmed-meshheading:16046526-Antigens, CD,
pubmed-meshheading:16046526-Case-Control Studies,
pubmed-meshheading:16046526-Cytotoxicity Tests, Immunologic,
pubmed-meshheading:16046526-Female,
pubmed-meshheading:16046526-HLA Antigens,
pubmed-meshheading:16046526-Histocompatibility Antigens Class I,
pubmed-meshheading:16046526-Histocompatibility Testing,
pubmed-meshheading:16046526-Humans,
pubmed-meshheading:16046526-Killer Cells, Natural,
pubmed-meshheading:16046526-Leukemia, Myelogenous, Chronic, BCR-ABL Positive,
pubmed-meshheading:16046526-Male,
pubmed-meshheading:16046526-NK Cell Lectin-Like Receptor Subfamily K,
pubmed-meshheading:16046526-Neoplastic Stem Cells,
pubmed-meshheading:16046526-Receptors, Immunologic,
pubmed-meshheading:16046526-Receptors, Natural Killer Cell,
pubmed-meshheading:16046526-T-Lymphocytes,
pubmed-meshheading:16046526-Tumor Cells, Cultured
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pubmed:year |
2005
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pubmed:articleTitle |
The antileukemia effect of HLA-matched NK and NK-T cells in chronic myelogenous leukemia involves NKG2D-target-cell interactions.
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pubmed:affiliation |
Stem Cell Allotransplantation Section, Hematology Branch, National Heart Lung and Blood Institute, Department of Transfusion Medicine, Clinical Center, National Institutes of Health (NIH), Bethesda, MD 20892, USA.
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pubmed:publicationType |
Journal Article
|