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10.1172/JCI74347 http://scihub22266oqcxt.onion/10.1172/JCI74347 C4362225!4362225!25642768     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Clin+Invest 2015 ; 125 (3): 1069-80 Nephropedia Template TP {{tp|p=25642768|t=2015. MicroRNA-21 promotes Th17 differentiation and mediates experimental autoimmune encephalomyelitis |pdf=|usr=}}{{25642768}} gab.com Text MicroRNA-21 promotes Th17 differentiation and mediates experimental autoimmune encephalomyelitis JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=25642768 #FOAvip Accumulation of IL-17?producing Th17 cells is associated with the development of multiple autoimmune diseases; however, the contribution of microRNA (miRNA) pathways to the intrinsic control of Th17 development remains unclear. Here, we demonstrated that miR-21 expression is elevated in Th17 cells and that mice lacking miR-21 have a defect in Th17 differentiation and are resistant to experimental autoimmune encephalomyelitis (EAE). Furthermore, we determined that miR-21 promotes Th17 differentiation by targeting and depleting SMAD-7, a negative regulator of TGF-? signaling. Moreover, the decreases in Th17 differentiation in miR-21?deficient T cells were associated with defects in SMAD-2/3 activation and IL-2 suppression. Finally, we found that treatment of WT mice with an anti?miR-21 oligonucleotide reduced the clinical severity of EAE, which was associated with a decrease in Th17 cells. Thus, we have characterized a T cell?intrinsic miRNA pathway that enhances TGF-? signaling, limits the autocrine inhibitory effects of IL-2, and thereby promotes Th17 differentiation and autoimmunity. Twit Text FOAVip MicroRNA-21 promotes Th17 differentiation and mediates experimental autoimmune encephalomyelitis ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=25642768 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25642768 #FOAvip English Wikipedia <ref>{{Cite pmid|25642768}}</ref> MicroRNA-21 promotes Th17 differentiation and mediates experimental autoimmune encephalomyelitis #MMPMID25642768 Murugaiyan G; da Cunha AP; Ajay AK; Joller N; Garo LP; Kumaradevan S; Yosef N; Vaidya VS; Weiner HL J Clin Invest 2015[Mar]; 125 (3): 1069-80 PMID25642768show ga Accumulation of IL-17?producing Th17 cells is associated with the development of multiple autoimmune diseases; however, the contribution of microRNA (miRNA) pathways to the intrinsic control of Th17 development remains unclear. Here, we demonstrated that miR-21 expression is elevated in Th17 cells and that mice lacking miR-21 have a defect in Th17 differentiation and are resistant to experimental autoimmune encephalomyelitis (EAE). Furthermore, we determined that miR-21 promotes Th17 differentiation by targeting and depleting SMAD-7, a negative regulator of TGF-? signaling. Moreover, the decreases in Th17 differentiation in miR-21?deficient T cells were associated with defects in SMAD-2/3 activation and IL-2 suppression. Finally, we found that treatment of WT mice with an anti?miR-21 oligonucleotide reduced the clinical severity of EAE, which was associated with a decrease in Th17 cells. Thus, we have characterized a T cell?intrinsic miRNA pathway that enhances TGF-? signaling, limits the autocrine inhibitory effects of IL-2, and thereby promotes Th17 differentiation and autoimmunity. äMicroRNA-21 promotes Th17 differentiation and mediates experimental au(epmc).pdf DeepDyve Pubget Overpricing