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rdf:type |
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lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0022688,
umls-concept:C0031715,
umls-concept:C0185117,
umls-concept:C0254610,
umls-concept:C0332161,
umls-concept:C0567416,
umls-concept:C0596402,
umls-concept:C1335872,
umls-concept:C1366765,
umls-concept:C1425775,
umls-concept:C1511636,
umls-concept:C2911684
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pubmed:issue |
1
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pubmed:dateCreated |
2008-4-2
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pubmed:abstractText |
NK cells are crucial components of the innate immune system, providing a first line of defense against infectious pathogens and tumors. IL-15 is the major physiologic growth factor responsible for NK cell differentiation, survival and cytolytic activity of mature NK cells. However, the exact regulatory mechanism of IL-15 on NK cell function is still unclear. In this study, we try to investigate the mechanism of IL-15 on NK cytolysis. Our results demonstrate that IL-15 treatment increased NKG2D transcripts and surface expression in NK cells. NKG2D or MICA blockade attenuated the up-regulation of IL-15 on NK cytolysis, demonstrating that the up-regulatory effect of IL-15 on NK cytolysis is at least partly dependent of the interaction of NKG2D and MICA. Furthermore, IL-15 augmented the expression of cytotoxic effector molecules (TRAIL and Perforin) and the phosphorylation of STAT1 and ERK1/2, which may also contribute the NK lysis. These results may have therapeutic implications when designing cytokine immunotherapy against cancer.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class I,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-15,
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/Mitogen-Activated Protein Kinase 1,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 3,
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,
http://linkedlifedata.com/resource/pubmed/chemical/STAT1 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/STAT1 protein, human
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1096-0023
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
42
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
128-36
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:18280748-Animals,
pubmed-meshheading:18280748-Cell Line,
pubmed-meshheading:18280748-Coculture Techniques,
pubmed-meshheading:18280748-Cytotoxicity, Immunologic,
pubmed-meshheading:18280748-Histocompatibility Antigens Class I,
pubmed-meshheading:18280748-Humans,
pubmed-meshheading:18280748-Immunity, Innate,
pubmed-meshheading:18280748-Interferon-gamma,
pubmed-meshheading:18280748-Interleukin-15,
pubmed-meshheading:18280748-Killer Cells, Natural,
pubmed-meshheading:18280748-Mitogen-Activated Protein Kinase 1,
pubmed-meshheading:18280748-Mitogen-Activated Protein Kinase 3,
pubmed-meshheading:18280748-NK Cell Lectin-Like Receptor Subfamily K,
pubmed-meshheading:18280748-Phosphorylation,
pubmed-meshheading:18280748-Receptors, Immunologic,
pubmed-meshheading:18280748-Receptors, Natural Killer Cell,
pubmed-meshheading:18280748-STAT1 Transcription Factor
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pubmed:year |
2008
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pubmed:articleTitle |
Interleukin-15 improves cytotoxicity of natural killer cells via up-regulating NKG2D and cytotoxic effector molecule expression as well as STAT1 and ERK1/2 phosphorylation.
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pubmed:affiliation |
Institute of Immunopharmacology & Immunotherapy, School of Pharmaceutical Sciences, Shandong University, 44 Wenhua West Road, Jinan 250012, China. caizhangsd@yahoo.com.cn
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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