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10.1371/journal.pone.0144090 http://scihub22266oqcxt.onion/10.1371/journal.pone.0144090 C4666626!4666626!26624013     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+One 2015 ; 10 (12): ä Nephropedia Template TP {{tp|p=26624013|t=2015. E2-2 Dependent Plasmacytoid Dendritic Cells Control Autoimmune Diabetes |pdf=|usr=}}{{26624013}} gab.com Text E2-2 Dependent Plasmacytoid Dendritic Cells Control Autoimmune Diabetes JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26624013 #FOAvip Autoimmune diabetes is a consequence of immune-cell infiltration and destruction of pancreatic ?-cells in the islets of Langerhans. We analyzed the cellular composition of the insulitic lesions in the autoimmune-prone non-obese diabetic (NOD) mouse and observed a peak in recruitment of plasmacytoid dendritic cells (pDCs) to NOD islets around 8?9 weeks of age. This peak coincides with increased spontaneous expression of type-1-IFN response genes and CpG1585 induced production of IFN-? from NOD islets. The transcription factor E2-2 is specifically required for the maturation of pDCs, and we show that knocking out E2-2 conditionally in CD11c+ cells leads to a reduced recruitment of pDCs to pancreatic islets and reduced CpG1585 induced production of IFN-? during insulitis. As a consequence, insulitis has a less aggressive expression profile of the Th1 cytokine IFN-? and a markedly reduced diabetes incidence. Collectively, these observations demonstrate a disease-promoting role of E2-2 dependent pDCs in the pancreas during autoimmune diabetes in the NOD mouse. Twit Text FOAVip E2-2 Dependent Plasmacytoid Dendritic Cells Control Autoimmune Diabetes ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26624013 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26624013 #FOAvip English Wikipedia <ref>{{Cite pmid|26624013}}</ref> E2-2 Dependent Plasmacytoid Dendritic Cells Control Autoimmune Diabetes #MMPMID26624013 Hansen L; Schmidt-Christensen A; Gupta S; Fransén-Pettersson N; Hannibal TD; Reizis B; Santamaria P; Holmberg D PLoS One 2015[]; 10 (12): ä PMID26624013show ga Autoimmune diabetes is a consequence of immune-cell infiltration and destruction of pancreatic ?-cells in the islets of Langerhans. We analyzed the cellular composition of the insulitic lesions in the autoimmune-prone non-obese diabetic (NOD) mouse and observed a peak in recruitment of plasmacytoid dendritic cells (pDCs) to NOD islets around 8?9 weeks of age. This peak coincides with increased spontaneous expression of type-1-IFN response genes and CpG1585 induced production of IFN-? from NOD islets. The transcription factor E2-2 is specifically required for the maturation of pDCs, and we show that knocking out E2-2 conditionally in CD11c+ cells leads to a reduced recruitment of pDCs to pancreatic islets and reduced CpG1585 induced production of IFN-? during insulitis. As a consequence, insulitis has a less aggressive expression profile of the Th1 cytokine IFN-? and a markedly reduced diabetes incidence. Collectively, these observations demonstrate a disease-promoting role of E2-2 dependent pDCs in the pancreas during autoimmune diabetes in the NOD mouse. äE2-2 Dependent Plasmacytoid Dendritic Cells Control Autoimmune Diabete(epmc).pdf DeepDyve Pubget Overpricing