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10.1016/j.celrep.2016.10.042 http://scihub22266oqcxt.onion/10.1016/j.celrep.2016.10.042 C5108556!5108556 !27829150     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27829150 &cmd=llinks): Failed to open stream: HTTP request failed! 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Programmed Death-1 Culls Peripheral Accumulation of High-Affinity Autoreactive CD4 T Cells to Protect against Autoimmunity |pdf=|usr=}}{{27829150 }} gab.com Text Programmed Death-1 Culls Peripheral Accumulation of High-Affinity Autoreactive CD4 T Cells to Protect against Autoimmunity JO: Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=27829150 #FOAvip Self-reactive CD4 T cells are incompletely deleted during thymic development, and their peripheral seeding highlights the need for additional safeguards to avert autoimmunity. Here, we show an essential role for the coinhibitory molecule programmed death-1 (PD-1) in silencing the activation of high-affinity autoreactive CD4 T cells. Each wave of self-reactive CD4 T cells that escapes thymic deletion autonomously upregulates PD-1 to maintain self-tolerance. By tracking the progeny derived from individual autoreactive CD4 T cell clones, we demonstrate that self-reactive cells with the greatest autoimmune threat and highest self-antigen affinity express the most PD-1. Reciprocally, PD-1 deprivation unleashes high-affinity self-reactive CD4 T cells in target tissues to exacerbate neuronal inflammation and autoimmune diabetes. Reliance on PD-1 to actively maintain self-tolerance may explain why exploiting this pathway by cancerous cells and invasive microbes efficiently subverts protective immunity, and why autoimmune side effects can develop after PD-1-neutralizing checkpoint therapies. Twit Text FOAVip Programmed Death-1 Culls Peripheral Accumulation of High-Affinity Autoreactive CD4 T Cells to Protect against Autoimmunity ????Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=27829150 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27829150 #FOAvip English Wikipedia <ref>{{Cite pmid|27829150 }}</ref> Programmed Death-1 Culls Peripheral Accumulation of High-Affinity Autoreactive CD4 T Cells to Protect against Autoimmunity #MMPMID27829150 Jiang TT ; Martinov T ; Xin L ; Kinder JM ; Spanier JA ; Fife BT ; Way SS Cell Rep 2016[Nov]; 17 (7 ): 1783-1794 PMID27829150 show ga Self-reactive CD4 T cells are incompletely deleted during thymic development, and their peripheral seeding highlights the need for additional safeguards to avert autoimmunity. Here, we show an essential role for the coinhibitory molecule programmed death-1 (PD-1) in silencing the activation of high-affinity autoreactive CD4 T cells. Each wave of self-reactive CD4 T cells that escapes thymic deletion autonomously upregulates PD-1 to maintain self-tolerance. By tracking the progeny derived from individual autoreactive CD4 T cell clones, we demonstrate that self-reactive cells with the greatest autoimmune threat and highest self-antigen affinity express the most PD-1. Reciprocally, PD-1 deprivation unleashes high-affinity self-reactive CD4 T cells in target tissues to exacerbate neuronal inflammation and autoimmune diabetes. Reliance on PD-1 to actively maintain self-tolerance may explain why exploiting this pathway by cancerous cells and invasive microbes efficiently subverts protective immunity, and why autoimmune side effects can develop after PD-1-neutralizing checkpoint therapies. |*Autoimmunity [MESH] |Animals [MESH] |Autoantigens/immunology [MESH] |CD4-Positive T-Lymphocytes/*immunology [MESH] |Cell Proliferation [MESH] |Clone Cells [MESH] |Lymphocyte Activation/immunology [MESH] |Mice, Inbred C57BL [MESH] |Programmed Cell Death 1 Receptor/*metabolism [MESH] |Receptors, Antigen, T-Cell/metabolism [MESH]Programmed Death-1 Culls Peripheral Accumulation of High-Affinity Auto(epmc).pdf DeepDyve Pubget Overpricing