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rdf:type |
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lifeskim:mentions |
umls-concept:C0007613,
umls-concept:C0011306,
umls-concept:C0021469,
umls-concept:C0022688,
umls-concept:C0042769,
umls-concept:C0181586,
umls-concept:C0205160,
umls-concept:C0205349,
umls-concept:C0220847,
umls-concept:C0382839,
umls-concept:C0441655,
umls-concept:C0524910,
umls-concept:C0597357,
umls-concept:C0851285,
umls-concept:C1709059,
umls-concept:C1834367
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pubmed:issue |
10
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pubmed:dateCreated |
2004-11-5
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pubmed:abstractText |
NK cells are potent activators of dendritic cells (DCs), but it remains obscure how third-party cells affect the ability of NK cells to modulate DC functions. We show here that NK cells derived from healthy donors (N-NK), when cocultured with human liver epithelial cells, induced maturation as well as activation of DCs, such as increased migratory capacity as well as T cell stimulatory activity. In contrast, NK cells from chronic hepatitis C virus-infected donors (HCV-NK) were not capable of activating DCs under the same conditions. In comparison to N-NK, HCV-NK showed higher expression of CD94/NKG2A and produced IL-10 and TGFbeta when cultured with hepatic cells, most of which express HLA-E, a ligand for CD94/NKG2A. Blockade of NKG2A restored the ability of HCV-NK to activate DCs, which appeared to result from the reduced NK cell production of IL-10 and TGFbeta. The blockade also endowed HCV-NK with an ability to drive DCs to generate Th1-polarized CD4+ T cells. These findings show that NK cell modulation of DCs is regulated by third-party cells through NK receptor and its ligand interaction. Aberrant expression of NK receptors may have an impact on the magnitude and direction of DC activation of T cells under pathological conditions, such as chronic viral 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/HLA Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/HLA-E antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class I,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/KLRC1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/KLRD1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Lectins, C-Type,
http://linkedlifedata.com/resource/pubmed/chemical/NK Cell Lectin-Like Receptor...,
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/Suppressor Factors, Immunologic,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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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 |
15
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pubmed:volume |
173
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6072-81
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:15528343-Antigens, CD,
pubmed-meshheading:15528343-Cell Differentiation,
pubmed-meshheading:15528343-Cell Line, Tumor,
pubmed-meshheading:15528343-Cell-Free System,
pubmed-meshheading:15528343-Cells, Cultured,
pubmed-meshheading:15528343-Coculture Techniques,
pubmed-meshheading:15528343-Cytotoxicity, Immunologic,
pubmed-meshheading:15528343-Dendritic Cells,
pubmed-meshheading:15528343-Down-Regulation,
pubmed-meshheading:15528343-HLA Antigens,
pubmed-meshheading:15528343-Hepatitis C, Chronic,
pubmed-meshheading:15528343-Histocompatibility Antigens Class I,
pubmed-meshheading:15528343-Humans,
pubmed-meshheading:15528343-Immunophenotyping,
pubmed-meshheading:15528343-Interleukin-10,
pubmed-meshheading:15528343-K562 Cells,
pubmed-meshheading:15528343-Killer Cells, Natural,
pubmed-meshheading:15528343-Lectins, C-Type,
pubmed-meshheading:15528343-Lymphocyte Activation,
pubmed-meshheading:15528343-Lymphocyte Count,
pubmed-meshheading:15528343-NK Cell Lectin-Like Receptor Subfamily C,
pubmed-meshheading:15528343-NK Cell Lectin-Like Receptor Subfamily D,
pubmed-meshheading:15528343-Receptors, Immunologic,
pubmed-meshheading:15528343-Receptors, Natural Killer Cell,
pubmed-meshheading:15528343-Signal Transduction,
pubmed-meshheading:15528343-Suppressor Factors, Immunologic,
pubmed-meshheading:15528343-Transforming Growth Factor beta,
pubmed-meshheading:15528343-Up-Regulation
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pubmed:year |
2004
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pubmed:articleTitle |
Negative regulation of NK cell activities by inhibitory receptor CD94/NKG2A leads to altered NK cell-induced modulation of dendritic cell functions in chronic hepatitis C virus infection.
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pubmed:affiliation |
Department of Molecular Therapeutics, Osaka University Graduate School of Medicine, Yamadaoka 2-2, Suita, Osaka 565-0871, Japan.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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