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10.1126/science.1258867 http://scihub22266oqcxt.onion/10.1126/science.1258867 C4856222!4856222 !25745066     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25745066 &cmd=llinks): Failed to open stream: HTTP request failed! 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Antitumor immunity A shed NKG2D ligand that promotes natural killer cell activation and tumor rejection |pdf=|usr=}}{{25745066 }} gab.com Text Antitumor immunity A shed NKG2D ligand that promotes natural killer cell activation and tumor rejection JO: Science http://www.kidney.de/pget.php?&tw=1&pmid=25745066 #FOAvip Immune cells, including natural killer (NK) cells, recognize transformed cells and eliminate them in a process termed immunosurveillance. It is thought that tumor cells evade immunosurveillance by shedding membrane ligands that bind to the NKG2D-activating receptor on NK cells and/or T cells, and desensitize these cells. In contrast, we show that in mice, a shed form of MULT1, a high-affinity NKG2D ligand, causes NK cell activation and tumor rejection. Recombinant soluble MULT1 stimulated tumor rejection in mice. Soluble MULT1 functions, at least in part, by competitively reversing a global desensitization of NK cells imposed by engagement of membrane NKG2D ligands on tumor-associated cells, such as myeloid cells. The results overturn conventional wisdom that soluble ligands are always inhibitory and suggest a new approach for cancer immunotherapy. Twit Text FOAVip Antitumor immunity A shed NKG2D ligand that promotes natural killer cell activation and tumor rejection ????Science http://www.kidney.de/pget.php?&tw=1&pmid=25745066 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25745066 #FOAvip English Wikipedia <ref>{{Cite pmid|25745066 }}</ref> Antitumor immunity A shed NKG2D ligand that promotes natural killer cell activation and tumor rejection #MMPMID25745066 Deng W ; Gowen BG ; Zhang L ; Wang L ; Lau S ; Iannello A ; Xu J ; Rovis TL ; Xiong N ; Raulet DH Science 2015[Apr]; 348 (6230 ): 136-9 PMID25745066 show ga Immune cells, including natural killer (NK) cells, recognize transformed cells and eliminate them in a process termed immunosurveillance. It is thought that tumor cells evade immunosurveillance by shedding membrane ligands that bind to the NKG2D-activating receptor on NK cells and/or T cells, and desensitize these cells. In contrast, we show that in mice, a shed form of MULT1, a high-affinity NKG2D ligand, causes NK cell activation and tumor rejection. Recombinant soluble MULT1 stimulated tumor rejection in mice. Soluble MULT1 functions, at least in part, by competitively reversing a global desensitization of NK cells imposed by engagement of membrane NKG2D ligands on tumor-associated cells, such as myeloid cells. The results overturn conventional wisdom that soluble ligands are always inhibitory and suggest a new approach for cancer immunotherapy. |Animals [MESH] |Carrier Proteins/genetics/*immunology/pharmacology [MESH] |Histocompatibility Antigens Class I/genetics/*immunology/pharmacology [MESH] |Immunologic Surveillance [MESH] |Immunotherapy/methods [MESH] |Killer Cells, Natural/*immunology [MESH] |Ligands [MESH] |Lymphocyte Activation [MESH] |Melanoma, Experimental/immunology/therapy [MESH] |Membrane Proteins [MESH] |Mice [MESH] |NK Cell Lectin-Like Receptor Subfamily K/*immunology [MESH] |Neoplasms/*immunology/therapy [MESH] |Recombinant Proteins/genetics/immunology/pharmacology [MESH]Antitumor immunity A shed NKG2D ligand that promotes natural killer c(epmc).pdf DeepDyve Pubget Overpricing