Source:http://linkedlifedata.com/resource/pubmed/id/19454667
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0022688,
umls-concept:C0185117,
umls-concept:C0205245,
umls-concept:C0205263,
umls-concept:C0443199,
umls-concept:C0567416,
umls-concept:C0851285,
umls-concept:C0936012,
umls-concept:C1416652,
umls-concept:C1416654,
umls-concept:C1515021,
umls-concept:C1948023,
umls-concept:C2911684
|
pubmed:issue |
11
|
pubmed:dateCreated |
2009-5-20
|
pubmed:abstractText |
Recently, the Z27 mAb was shown to recognize the NK cell-activating receptor KIR3DS1, and several genetic studies suggest that the most probable ligands of KIR3DS1 are HLA class I molecules with the Bw4 motif. Despite these findings, the attempts to establish a functional interaction between KIR3DS1 and its potential ligand have been unsuccessful. Here, we study the proliferation and cytotoxicity of KIR3DS1(+) NK cells, compared with KIR3DL1(+) NK cells, according to the Bw4(+) or Bw4(-) allogeneic environment. Our results show for the first time that KIR3DS1 expression on NK cells can be induced after exposure to stimulator cells (221, K562, EBV-B cell lines, and B cells), polyinosinic-polycytidylic acid, IL-15, or IL-2. Furthermore, whereas KIR3DL1(+) NK cell proliferation and cytotoxicity were inhibited in a Bw4(+) but not a Bw4(-) context, KIR3DS1(+) NK cell functions were not influenced by the presence of Bw4 on target cells. Nevertheless, despite the absence of demonstrated regulation of KIR3DS1(+) NK cell functions by HLA-Bw4 molecules, we found a higher KIR3DS1(+) NK cell frequency and higher levels of KIR3DS1 expression in Bw4(+) compared with Bw4(-) individuals. Altogether, these results suggest that KIR3DS1 does not recognize HLA-Bw4 molecules in a physiological context, and they highlight the induced expression of KIR3DS1 observed on stimulated NK cells and the higher frequency of KIR3DS1(+) NK cells in Bw4(+) individuals. Because a protective KIR3DS1-Bw4 association has been reported in viral infections, our results further the understanding of the role of KIR3DS1(+) NK cells in controlling viral infections.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
AIM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/HLA-B Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/HLA-Bw4 antigen,
http://linkedlifedata.com/resource/pubmed/chemical/KIR3DL1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, KIR3DL1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, KIR3DS1
|
pubmed:status |
MEDLINE
|
pubmed:month |
Jun
|
pubmed:issn |
1550-6606
|
pubmed:author | |
pubmed:issnType |
Electronic
|
pubmed:day |
1
|
pubmed:volume |
182
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
6727-35
|
pubmed:dateRevised |
2011-11-17
|
pubmed:meshHeading |
pubmed-meshheading:19454667-Cell Proliferation,
pubmed-meshheading:19454667-Cytotoxicity, Immunologic,
pubmed-meshheading:19454667-Gene Expression Regulation,
pubmed-meshheading:19454667-HLA-B Antigens,
pubmed-meshheading:19454667-Humans,
pubmed-meshheading:19454667-K562 Cells,
pubmed-meshheading:19454667-Lymphocyte Activation,
pubmed-meshheading:19454667-Natural Killer T-Cells,
pubmed-meshheading:19454667-Receptors, KIR3DL1,
pubmed-meshheading:19454667-Receptors, KIR3DS1,
pubmed-meshheading:19454667-T-Lymphocyte Subsets
|
pubmed:year |
2009
|
pubmed:articleTitle |
Phenotypic and functional analyses of KIR3DL1+ and KIR3DS1+ NK cell subsets demonstrate differential regulation by Bw4 molecules and induced KIR3DS1 expression on stimulated NK cells.
|
pubmed:affiliation |
Etablissement Français du Sang, Université de Nantes, ImmunoVirologie et Polymorphisme Génétique, Nantes, France.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|