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10.1073/pnas.1418316112 http://scihub22266oqcxt.onion/10.1073/pnas.1418316112 C4386391!4386391!25775512     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Proc+Natl+Acad+Sci+U+S+A 2015 ; 112 (13): 4080-5 Nephropedia Template TP {{tp|p=25775512|t=2015. Glucocorticoid-resistant Th17 cells are selectively attenuated by cyclosporine A |pdf=|usr=}}{{25775512}} gab.com Text Glucocorticoid-resistant Th17 cells are selectively attenuated by cyclosporine A JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=25775512 #FOAvip Cyclosporine A was one of the first drugs used in clinical practice to successfully rescue glucocorticoid-resistant inflammatory diseases. In this article we extend the characterization of glucocorticoid-resistant human Th17 cells, and demonstrate that this effector memory T-cell subset is reciprocally attenuated by cyclosporine A. This therapeutic paradigm was confirmed in a murine model of autoimmunity, refining our understanding of cyclosporine A?s effect on the adaptive immune response. These data support the rationale for Th17-targeting therapies in the treatment of glucocorticoid-resistant inflammation. Twit Text FOAVip Glucocorticoid-resistant Th17 cells are selectively attenuated by cyclosporine A ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=25775512 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25775512 #FOAvip English Wikipedia <ref>{{Cite pmid|25775512}}</ref> Glucocorticoid-resistant Th17 cells are selectively attenuated by cyclosporine A #MMPMID25775512 Schewitz-Bowers LP; Lait PJP; Copland DA; Chen P; Wu W; Dhanda AD; Vistica BP; Williams EL; Liu B; Jawad S; Li Z; Tucker W; Hirani S; Wakabayashi Y; Zhu J; Sen N; Conway-Campbell BL; Gery I; Dick AD; Wei L; Nussenblatt RB; Lee RWJ Proc Natl Acad Sci U S A 2015[Mar]; 112 (13): 4080-5 PMID25775512show ga Cyclosporine A was one of the first drugs used in clinical practice to successfully rescue glucocorticoid-resistant inflammatory diseases. In this article we extend the characterization of glucocorticoid-resistant human Th17 cells, and demonstrate that this effector memory T-cell subset is reciprocally attenuated by cyclosporine A. This therapeutic paradigm was confirmed in a murine model of autoimmunity, refining our understanding of cyclosporine A?s effect on the adaptive immune response. These data support the rationale for Th17-targeting therapies in the treatment of glucocorticoid-resistant inflammation. äGlucocorticoid-resistant Th17 cells are selectively attenuated by cycl(epmc).pdf DeepDyve Pubget Overpricing