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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
2003-6-2
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pubmed:abstractText |
The cognate NK-DC interaction in inflamed tissues results in NK cell activation and acquisition of cytotoxicity against immature DC (iDC). This may represent a mechanism of DC selection required for the control of downstream adaptive immune responses. Here we show that killing of monocyte-derived iDC is confined to the NK cell subset that expresses CD94/NKG2A, but not killer Ig-like receptors (KIR). Consistent with these data, the expression of HLA-E (i.e. the cellular ligand of CD94/NKG2A) was down-regulated in iDC. On the other hand, HLA-B and HLA-C down-regulation in iDC was not sufficient to induce cytotoxicity in NK cells expressing KIR3DL1 or KIR2DL. Remarkably, CD94/NKG2A(+)KIR(-) NK cells were heterogeneous in their ability to kill iDC and an inverse correlation existed between their CD94/NKG2A surface density and the magnitude of their cytolytic activity. It is conceivable that the reduced CD94/NKG2A surface density enables these cells to efficiently sense the decrease of HLA-E surface expression in iDC. Finally, most NK cells that lysed iDC did not kill mature DC that express higher amounts of HLA class I molecules (including HLA-E)as compared with iDC. However, a small NK cell subset was capable of killing not only iDC but also mature DC.
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pubmed:commentsCorrections |
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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/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/HLA Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/HLA-B Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/HLA-C 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/KIR3DL1 protein, human,
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, KIR,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, KIR3DL1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Natural Killer Cell
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0014-2980
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
33
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1657-66
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:12778484-Antigens, CD,
pubmed-meshheading:12778484-Cells, Cultured,
pubmed-meshheading:12778484-Cytotoxicity, Immunologic,
pubmed-meshheading:12778484-Dendritic Cells,
pubmed-meshheading:12778484-HLA Antigens,
pubmed-meshheading:12778484-HLA-B Antigens,
pubmed-meshheading:12778484-HLA-C Antigens,
pubmed-meshheading:12778484-Histocompatibility Antigens Class I,
pubmed-meshheading:12778484-Humans,
pubmed-meshheading:12778484-Killer Cells, Natural,
pubmed-meshheading:12778484-Lectins, C-Type,
pubmed-meshheading:12778484-NK Cell Lectin-Like Receptor Subfamily C,
pubmed-meshheading:12778484-NK Cell Lectin-Like Receptor Subfamily D,
pubmed-meshheading:12778484-Receptors, Immunologic,
pubmed-meshheading:12778484-Receptors, KIR,
pubmed-meshheading:12778484-Receptors, KIR3DL1,
pubmed-meshheading:12778484-Receptors, Natural Killer Cell
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pubmed:year |
2003
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pubmed:articleTitle |
The natural killer cell-mediated killing of autologous dendritic cells is confined to a cell subset expressing CD94/NKG2A, but lacking inhibitory killer Ig-like receptors.
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pubmed:affiliation |
Dipartimento di Medicina Sperimentale, Università degli Studi di Genova, Italy.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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