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rdf:type |
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lifeskim:mentions |
umls-concept:C0011306,
umls-concept:C0017262,
umls-concept:C0035820,
umls-concept:C0042769,
umls-concept:C0185117,
umls-concept:C0220847,
umls-concept:C0389061,
umls-concept:C0524910,
umls-concept:C0684336,
umls-concept:C1155064,
umls-concept:C1511545,
umls-concept:C2911684
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pubmed:issue |
3
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pubmed:dateCreated |
2003-1-22
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pubmed:abstractText |
Dendritic cells (DCs) augment effector functions of NK cells, but the underlying mechanisms are not fully understood. Here we show in an in vitro coculture system that human monocyte-derived DCs enhance IFN-gamma production, CD69 expression, and K562 cytolytic ability of NK cells when DCs are prestimulated with various maturation stimuli such as IFN-alpha or LPS. Of interest is the finding that NK cell activation mediated by LPS-stimulated DCs was dependent on IL-12 produced in DC/NK coculture, but that IFN-alpha-stimulated DC-mediated activation was not. Alternatively, MHC class I-related chain A and B (MICA/B), ligands for NKG2D activating receptor, were found to be induced on DCs upon IFN-alpha stimulation and to be responsible for the NK activation because mAb-mediated masking of MICA/B as well as inhibition of direct cell-to-cell contact using transwell insert completely abolished DC-dependent NK cell activation by IFN-alpha. Finally, DCs recovered from chronic hepatitis C virus-infected patients showed defects in the induction of MICA/B and impaired ability to activate NK cells in response to IFN-alpha stimulation. These findings suggested that MICA/B induction on DCs may be one of the mechanisms by which IFN-alpha activates NK cells; this impairment might affect IFN-alpha responsiveness in hepatitis C virus infection.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation...,
http://linkedlifedata.com/resource/pubmed/chemical/CD69 antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class I,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-12,
http://linkedlifedata.com/resource/pubmed/chemical/Lectins, C-Type,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
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/Protein Subunits
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0022-1767
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
170
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1249-56
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:12538683-Antigens, CD,
pubmed-meshheading:12538683-Antigens, Differentiation, T-Lymphocyte,
pubmed-meshheading:12538683-Cell Communication,
pubmed-meshheading:12538683-Cell Differentiation,
pubmed-meshheading:12538683-Cells, Cultured,
pubmed-meshheading:12538683-Coculture Techniques,
pubmed-meshheading:12538683-Cytotoxicity, Immunologic,
pubmed-meshheading:12538683-Dendritic Cells,
pubmed-meshheading:12538683-Hepacivirus,
pubmed-meshheading:12538683-Hepatitis C, Chronic,
pubmed-meshheading:12538683-Histocompatibility Antigens Class I,
pubmed-meshheading:12538683-Humans,
pubmed-meshheading:12538683-Interferon-alpha,
pubmed-meshheading:12538683-Interferon-gamma,
pubmed-meshheading:12538683-Interleukin-12,
pubmed-meshheading:12538683-K562 Cells,
pubmed-meshheading:12538683-Killer Cells, Natural,
pubmed-meshheading:12538683-Lectins, C-Type,
pubmed-meshheading:12538683-Lipopolysaccharides,
pubmed-meshheading:12538683-Lymphocyte Activation,
pubmed-meshheading:12538683-Protein Subunits
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pubmed:year |
2003
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pubmed:articleTitle |
Critical role of MHC class I-related chain A and B expression on IFN-alpha-stimulated dendritic cells in NK cell activation: impairment in chronic hepatitis C virus infection.
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pubmed:affiliation |
Department of Molecular Therapeutics, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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