http://purl.uniprot.org/citations/19830740 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/19830740 | http://www.w3.org/2000/01/rdf-schema#comment | "Soluble HLA class I (sHLA-I) molecules can regulate survival of NK cells and their anti-tumor killing activity. Herein, we have analysed whether interaction of sHLA-I with CD8 and/or different isoforms of killer Ig-like receptors (KIR) induced secretion of transforming growth factor (TGF)-beta1. CD8+KIR-NK cell clones secreted TGF-beta1 upon the interaction of sHLA-I with CD8 molecule. sHLA-Cw4 or sHLA-Cw3 alleles engaging inhibitory isoforms of KIR, namely KIR2DL1 or KIR2DL2, strongly downregulated TGF-beta1 production elicited through CD8. On the other hand, sHLA-Cw4 or sHLA-Cw3 alleles induced secretion of TGF-beta1 by ligation of stimulatory KIR2DS1 or KIR2DS2 isoforms. TGF-beta1 strongly reduced NK cell-mediated tumor cell lysis and production of pro-inflammatory cytokines such as TNF-alpha and IFN-gamma. Also, TGF-beta1 inhibited NK cell cytolysis induced by the engagement of stimulatory receptors including NKG2D, DNAM1, 2B4, CD69, NKp30, NKp44 and NKp46. The IL-2-dependent surface upregulation of some of these receptors was prevented by TGF-beta1. Furthermore, TGF-beta1 hampered IL-2-induced NK cell proliferation but not IL-2-mediated rescue from apoptosis of NK cells. Depletion of TGF-beta1 restored all the NK cell-mediated functional activities analysed. Taken together these findings suggest that sHLA-I antigens may downregulate the NK cell-mediated innate response by inducing TGF-beta1 release."xsd:string |
http://purl.uniprot.org/citations/19830740 | http://purl.org/dc/terms/identifier | "doi:10.1002/eji.200939728"xsd:string |
http://purl.uniprot.org/citations/19830740 | http://purl.uniprot.org/core/author | "Poggi A."xsd:string |
http://purl.uniprot.org/citations/19830740 | http://purl.uniprot.org/core/author | "Musso A."xsd:string |
http://purl.uniprot.org/citations/19830740 | http://purl.uniprot.org/core/author | "Contini P."xsd:string |
http://purl.uniprot.org/citations/19830740 | http://purl.uniprot.org/core/author | "Ghio M."xsd:string |
http://purl.uniprot.org/citations/19830740 | http://purl.uniprot.org/core/author | "Negrini S."xsd:string |
http://purl.uniprot.org/citations/19830740 | http://purl.uniprot.org/core/author | "Boero S."xsd:string |
http://purl.uniprot.org/citations/19830740 | http://purl.uniprot.org/core/date | "2009"xsd:gYear |
http://purl.uniprot.org/citations/19830740 | http://purl.uniprot.org/core/name | "Eur J Immunol"xsd:string |
http://purl.uniprot.org/citations/19830740 | http://purl.uniprot.org/core/pages | "3459-3468"xsd:string |
http://purl.uniprot.org/citations/19830740 | http://purl.uniprot.org/core/title | "Soluble HLA-I-mediated secretion of TGF-beta1 by human NK cells and consequent down-regulation of anti-tumor cytolytic activity."xsd:string |
http://purl.uniprot.org/citations/19830740 | http://purl.uniprot.org/core/volume | "39"xsd:string |
http://purl.uniprot.org/citations/19830740 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/19830740 |
http://purl.uniprot.org/citations/19830740 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/19830740 |
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