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10.4161/mabs.29758 http://scihub22266oqcxt.onion/10.4161/mabs.29758 C4622985!4622985 !25517314     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25517314 &cmd=llinks): Failed to open stream: HTTP request failed! 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Failure to upregulate cell surface PD-1 is associated with dysregulated stimulation of T cells by TGN1412-like CD28 superagonist |pdf=|usr=}}{{25517314 }} gab.com Text Failure to upregulate cell surface PD-1 is associated with dysregulated stimulation of T cells by TGN1412-like CD28 superagonist JO: MAbs http://www.kidney.de/pget.php?&tw=1&pmid=25517314 #FOAvip The CD28 superagonist (CD28SA) TGN1412 was administered to humans as an agent that can selectively activate and expand regulatory T cells but resulted in uncontrolled T cell activation accompanied by cytokine storm. The molecular mechanisms that underlie this uncontrolled T cell activation are unclear. Physiological activation of T cells leads to upregulation of not only activation molecules but also inhibitory receptors such as PD-1. We hypothesized that the uncontrolled activation of CD28SA-stimulated T cells is due to both the enhanced expression of activation molecules and the lack of or reduced inhibitory signals. In this study, we show that anti-CD3 antibody-stimulated human T cells undergo time-limited controlled DNA synthesis, proliferation and interleukin-2 secretion, accompanied by PD-1 expression. In contrast, CD28SA-activated T cells demonstrate uncontrolled activation parameters including enhanced expression of LFA-1 and CCR5 but fail to express PD-1 on the cell surface. We demonstrate the functional relevance of the lack of PD-1 mediated regulatory mechanism in CD28SA-stimulated T cells. Our findings provide a molecular explanation for the dysregulated activation of CD28SA-stimulated T cells and also highlight the potential for the use of differential expression of PD-1 as a biomarker of safety for T cell immunostimulatory biologics. Twit Text FOAVip Failure to upregulate cell surface PD-1 is associated with dysregulated stimulation of T cells by TGN1412-like CD28 superagonist ????MAbs http://www.kidney.de/pget.php?&tw=1&pmid=25517314 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25517314 #FOAvip English Wikipedia <ref>{{Cite pmid|25517314 }}</ref> Failure to upregulate cell surface PD-1 is associated with dysregulated stimulation of T cells by TGN1412-like CD28 superagonist #MMPMID25517314 Thaventhiran T ; Alhumeed N ; Yeang HX ; Sethu S ; Downey JS ; Alghanem AF ; Olayanju A ; Smith EL ; Cross MJ ; Webb SD ; Williams DP ; Bristow A ; Ball C ; Stebbings R ; Sathish JG MAbs 2014[]; 6 (5 ): 1290-9 PMID25517314 show ga The CD28 superagonist (CD28SA) TGN1412 was administered to humans as an agent that can selectively activate and expand regulatory T cells but resulted in uncontrolled T cell activation accompanied by cytokine storm. The molecular mechanisms that underlie this uncontrolled T cell activation are unclear. Physiological activation of T cells leads to upregulation of not only activation molecules but also inhibitory receptors such as PD-1. We hypothesized that the uncontrolled activation of CD28SA-stimulated T cells is due to both the enhanced expression of activation molecules and the lack of or reduced inhibitory signals. In this study, we show that anti-CD3 antibody-stimulated human T cells undergo time-limited controlled DNA synthesis, proliferation and interleukin-2 secretion, accompanied by PD-1 expression. In contrast, CD28SA-activated T cells demonstrate uncontrolled activation parameters including enhanced expression of LFA-1 and CCR5 but fail to express PD-1 on the cell surface. We demonstrate the functional relevance of the lack of PD-1 mediated regulatory mechanism in CD28SA-stimulated T cells. Our findings provide a molecular explanation for the dysregulated activation of CD28SA-stimulated T cells and also highlight the potential for the use of differential expression of PD-1 as a biomarker of safety for T cell immunostimulatory biologics. |Antibodies, Monoclonal, Humanized/*immunology/pharmacology [MESH] |Blotting, Western [MESH] |CD28 Antigens/agonists/*immunology/metabolism [MESH] |CD4-Positive T-Lymphocytes/drug effects/immunology/metabolism [MESH] |Cell Adhesion/drug effects/immunology [MESH] |Cell Movement/drug effects/immunology [MESH] |Cell Proliferation/drug effects [MESH] |Cells, Cultured [MESH] |Endothelial Cells/drug effects/immunology/metabolism [MESH] |Flow Cytometry [MESH] |Humans [MESH] |Immunologic Memory/immunology [MESH] |Lymphocyte Function-Associated Antigen-1/immunology/metabolism [MESH] |Membrane Proteins/*immunology/metabolism [MESH] |Microscopy, Fluorescence [MESH] |Programmed Cell Death 1 Receptor/*immunology/metabolism [MESH] |Receptors, CCR5/immunology/metabolism [MESH] |T-Lymphocytes/drug effects/*immunology/metabolism [MESH]Failure to upregulate cell surface PD-1 is associated with dysregulate(epmc).pdf DeepDyve Pubget Overpricing