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10.1016/j.jaut.2017.11.005 http://scihub22266oqcxt.onion/10.1016/j.jaut.2017.11.005 C5916452!5916452!29183643     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 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Autoimmun 2018 ; 89 (ä): 41-52 Nephropedia Template TP {{tp|p=29183643|t=2018. Selective targeting of pro-inflammatory Th1 cells by microRNA-148a-specific antagomirs in vivo |pdf=|usr=}}{{29183643}} gab.com Text Selective targeting of pro-inflammatory Th1 cells by microRNA-148a-specific antagomirs in vivo JO: J Autoimmun http://www.kidney.de/pget.php?&tw=1&pmid=29183643 #FOAvip In T lymphocytes, expression of miR-148a is induced by T-bet and Twist1, and is specific for pro-inflammatory Th1 cells. In these cells, miR-148a inhibits the expression of the pro-apoptotic protein Bim and promotes their survival. Here we use sequence-specific cholesterol-modified oligonucleotides against miR-148a (antagomir-148a) for the selective elimination of pro-inflammatory Th1 cells in vivo. In the murine model of transfer colitis, antagomir-148a treatment reduced the number of pro-inflammatory Th1 cells in the colon of colitic mice by 50% and inhibited miR-148a expression by 71% in the remaining Th1 cells. Expression of Bim protein in colonic Th1 cells was increased. Antagomir-148a-mediated reduction of Th1 cells resulted in a significant amelioration of colitis. The effect of antagomir-148a was selective for chronic inflammation. Antigen-specific memory Th cells that were generated by an acute immune reaction to nitrophenylacetyl-coupled chicken gamma globulin (NP-CGG) were not affected by treatment with antagomir-148a, both during the effector and the memory phase. In addition, antibody titers to NP-CGG were not altered. Thus, antagomir-148a might qualify as an effective drug to selectively deplete pro-inflammatory Th1 cells of chronic inflammation without affecting the protective immunological memory. Twit Text FOAVip Selective targeting of pro-inflammatory Th1 cells by microRNA-148a-specific antagomirs in vivo ????J Autoimmun http://www.kidney.de/pget.php?&tw=1&pmid=29183643 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29183643 #FOAvip English Wikipedia <ref>{{Cite pmid|29183643}}</ref> Selective targeting of pro-inflammatory Th1 cells by microRNA-148a-specific antagomirs in vivo #MMPMID29183643 Maschmeyer P; Petkau G; Siracusa F; Zimmermann J; Zügel F; Kühl AA; Lehmann K; Schimmelpfennig S; Weber M; Haftmann C; Riedel R; Bardua M; Heinz GA; Tran CL; Hoyer BF; Hiepe F; Herzog S; Wittmann J; Rajewsky N; Melchers FG; Chang HD; Radbruch A; Mashreghi MF J Autoimmun 2018[May]; 89 (ä): 41-52 PMID29183643show ga In T lymphocytes, expression of miR-148a is induced by T-bet and Twist1, and is specific for pro-inflammatory Th1 cells. In these cells, miR-148a inhibits the expression of the pro-apoptotic protein Bim and promotes their survival. Here we use sequence-specific cholesterol-modified oligonucleotides against miR-148a (antagomir-148a) for the selective elimination of pro-inflammatory Th1 cells in vivo. In the murine model of transfer colitis, antagomir-148a treatment reduced the number of pro-inflammatory Th1 cells in the colon of colitic mice by 50% and inhibited miR-148a expression by 71% in the remaining Th1 cells. Expression of Bim protein in colonic Th1 cells was increased. Antagomir-148a-mediated reduction of Th1 cells resulted in a significant amelioration of colitis. The effect of antagomir-148a was selective for chronic inflammation. Antigen-specific memory Th cells that were generated by an acute immune reaction to nitrophenylacetyl-coupled chicken gamma globulin (NP-CGG) were not affected by treatment with antagomir-148a, both during the effector and the memory phase. In addition, antibody titers to NP-CGG were not altered. Thus, antagomir-148a might qualify as an effective drug to selectively deplete pro-inflammatory Th1 cells of chronic inflammation without affecting the protective immunological memory. äSelective targeting of pro-inflammatory Th1 cells by microRNA-148a-spe(epmc).pdf DeepDyve Pubget Overpricing