Source:http://linkedlifedata.com/resource/pubmed/id/11454312
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2001-7-16
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pubmed:abstractText |
NK-92, a highly cytotoxic, interleukin-2 (IL-2)-dependent human natural killer (NK) cell line, has been of interest for basic and translational research. We report on a comprehensive analysis of NK-92 for factors implicated in NK cytotoxicity to elucidate factors underlying NK-92's high cytolytic activity and target range. Thus, we hope to develop a method to identify patients best suited to NK-92 immunotherapy. In addition, as a model system, we hope to increase understanding of the basis for the elevated activity exhibited by activated NK (ANK) cells. NK-92 exhibits an unusual receptor expression profile, expressing a relatively large number of activating (NKp30, NKp46, 2B4, NKGD, E, CD28) receptors. Conversely, it expresses few inhibitory receptors (NKGA/B, low levels of KIR2DL4, ILT-2), lacking most of the killer inhibitory receptors (KIRs) clonally expressed on normal NK cells. In addition, NK-92 expresses high levels of molecules involved in the perforin-granzyme cytolytic pathway as well as additional cytotoxic effector molecules including tumor necrosis factor (TNF)-superfamily members FasL, TRAIL, TWEAK, TNF-alpha, indicating the ability to kill via alternative mechanisms. NK-92 also expresses other molecules implicated immune effector cell regulation (CD80, CD86, CD40L, TRANCE) whose relevance in NK killing is unclear. This study provides initial data to develop a method to identify NK-92 susceptible cells (cells expressing ligands for NK-92 activating receptors ie CD48 for 2B4 and CD80/86 for CD28). Furthermore, this work suggests mechanisms that may contribute to ANK cell activity, including modulation of receptor expression to favor activation, up-regulation of cytotoxic effector molecules, and acquisition of new cytolytic pathways.
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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 |
Jun
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pubmed:issn |
1525-8165
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
10
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
369-83
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pubmed:dateRevised |
2004-11-17
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pubmed:meshHeading |
pubmed-meshheading:11454312-Cell Adhesion Molecules,
pubmed-meshheading:11454312-Cell Line,
pubmed-meshheading:11454312-Cytotoxicity, Immunologic,
pubmed-meshheading:11454312-Humans,
pubmed-meshheading:11454312-Immunophenotyping,
pubmed-meshheading:11454312-Killer Cells, Natural,
pubmed-meshheading:11454312-Lectins,
pubmed-meshheading:11454312-Lymphoma, Non-Hodgkin,
pubmed-meshheading:11454312-Multigene Family,
pubmed-meshheading:11454312-Receptors, Immunologic,
pubmed-meshheading:11454312-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:11454312-Tumor Necrosis Factor-alpha
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pubmed:year |
2001
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pubmed:articleTitle |
Factors regulating the cytotoxic activity of the human natural killer cell line, NK-92.
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pubmed:affiliation |
Section of Bone Marrow Transplant and Cell Therapy, Rush Presbyterian-St. Luke's Medical Center, Rush Medical School, Rush University Chicago, IL 60612, USA.
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pubmed:publicationType |
Journal Article
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