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10.11909/j.issn.1671-5411.2015.04.011 http://scihub22266oqcxt.onion/10.11909/j.issn.1671-5411.2015.04.011 C4554787!4554787!26345215     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Geriatr+Cardiol 2015 ; 12 (4): 388-93 Nephropedia Template TP {{tp|p=26345215|t=2015. Cilostazol inhibits plasmacytoid dendritic cell activation and antigen presentation |pdf=|usr=}}{{26345215}} gab.com Text Cilostazol inhibits plasmacytoid dendritic cell activation and antigen presentation JO: J Geriatr Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=26345215 #FOAvip Background: Cilostazol, an anti-platelet drug for treating coronary heart disease, has been reported to modulate immune cell functions. Plasmacytoid dendritic cells (pDCs) have been found to participate in the progression of atherosclerosis mainly through interferon ? (IFN-?) production. Whether cilostazol influences pDCs activation is still not clear. In this study, we aimed to investigate the effects of cilostazol on cell activation and antigen presentation of pDCs in vitro in this study. Methods: Peripheral blood mononuclear cells isolated by Ficoll centrifugation and pDCs sorted by flow cytometry were used in this study. After pretreated with cilostazol for 2 h, cells were stimulated with CpG-A, R848 or virus for 6 h or 20 h, or stimulated with CpG-B for 48 h and then co-cultured with naïve T cell for five days. Cytokines in supernatant and intracellular cytokines were analyzed by ELISA or flow cytometry respectively. Results: Our data indicated that cilostazol could inhibit IFN-? and tumor necrosis factor ? (TNF-?) production from pDCs in a dose-dependent manner. In addition, the ability of priming naïve T cells of pDCs was also impaired by cilostazol. The inhibitory effect was not due to cell killing since the viability of pDCs did not change upon cilostazol treatment. Conclusion: Cilostazol inhibits pDCs cell activation and antigen presentation in vitro, which may explain how cilostazol protects against atherosclerosis. Twit Text FOAVip Cilostazol inhibits plasmacytoid dendritic cell activation and antigen presentation ????J Geriatr Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=26345215 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26345215 #FOAvip English Wikipedia <ref>{{Cite pmid|26345215}}</ref> Cilostazol inhibits plasmacytoid dendritic cell activation and antigen presentation #MMPMID26345215 Sun F; Yin Z; Yu HS; Shi QX; Zhao B; Zhang LG; Wang SL J Geriatr Cardiol 2015[Jul]; 12 (4): 388-93 PMID26345215show ga Background: Cilostazol, an anti-platelet drug for treating coronary heart disease, has been reported to modulate immune cell functions. Plasmacytoid dendritic cells (pDCs) have been found to participate in the progression of atherosclerosis mainly through interferon ? (IFN-?) production. Whether cilostazol influences pDCs activation is still not clear. In this study, we aimed to investigate the effects of cilostazol on cell activation and antigen presentation of pDCs in vitro in this study. Methods: Peripheral blood mononuclear cells isolated by Ficoll centrifugation and pDCs sorted by flow cytometry were used in this study. After pretreated with cilostazol for 2 h, cells were stimulated with CpG-A, R848 or virus for 6 h or 20 h, or stimulated with CpG-B for 48 h and then co-cultured with naïve T cell for five days. Cytokines in supernatant and intracellular cytokines were analyzed by ELISA or flow cytometry respectively. Results: Our data indicated that cilostazol could inhibit IFN-? and tumor necrosis factor ? (TNF-?) production from pDCs in a dose-dependent manner. In addition, the ability of priming naïve T cells of pDCs was also impaired by cilostazol. The inhibitory effect was not due to cell killing since the viability of pDCs did not change upon cilostazol treatment. Conclusion: Cilostazol inhibits pDCs cell activation and antigen presentation in vitro, which may explain how cilostazol protects against atherosclerosis. äCilostazol inhibits plasmacytoid dendritic cell activation and antigen(epmc).pdf DeepDyve Pubget Overpricing