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10.1016/j.immuni.2014.09.017 http://scihub22266oqcxt.onion/10.1016/j.immuni.2014.09.017 C4221807!4221807!25367572     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25367572.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Immunity 2014 ; 41 (4): 555-66 Nephropedia Template TP {{tp|p=25367572|t=2014. The oncoprotein and transcriptional regulator Bcl-3 governs plasticity and pathogenicity of auto-immune T cells |pdf=|usr=}}{{25367572}} gab.com Text The oncoprotein and transcriptional regulator Bcl-3 governs plasticity and pathogenicity of auto-immune T cells JO: Immunity http://www.kidney.de/pget.php?&tw=1&pmid=25367572 #FOAvip Bcl-3 is an atypical member of the I?B family that modulates transcription in the nucleus via association with p50 (NF-?B1) or p52 (NF-?B2) homodimers. Despite evidence attesting to the overall physiologic importance of Bcl-3, little is known about its cell-specific functions or mechanisms. Here we demonstrate a T cell-intrinsic function of Bcl-3 in autoimmunity. Bcl-3-deficient T cells failed to induce disease in T cell transfer-induced colitis and experimental autoimmune encephalomyelitis. The protection against disease correlated with a decrease in Th1 cells that produced the cytokines IFN?- and GM-CSF, and an increase in Th17 cells. Although differentiation into Th1 cells was not impaired in the absence of Bcl-3, differentiated Th1 cells converted to less pathogenic Th17-like cells, in part via mechanisms involving expression of the ROR?t transcription factor. Thus, Bcl-3 constrained Th1 cell plasticity and promoted pathogenicity by blocking conversion to Th17-like cells, revealing a unique type of regulation that shapes adaptive immunity. Twit Text FOAVip The oncoprotein and transcriptional regulator Bcl-3 governs plasticity and pathogenicity of auto-immune T cells ????Immunity http://www.kidney.de/pget.php?&tw=1&pmid=25367572 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25367572 #FOAvip English Wikipedia <ref>{{Cite pmid|25367572}}</ref> The oncoprotein and transcriptional regulator Bcl-3 governs plasticity and pathogenicity of auto-immune T cells #MMPMID25367572 Tang W; Wang H; Claudio E; Tassi I; Ha Hl; Saret S; Siebenlist U Immunity 2014[Oct]; 41 (4): 555-66 PMID25367572show ga Bcl-3 is an atypical member of the I?B family that modulates transcription in the nucleus via association with p50 (NF-?B1) or p52 (NF-?B2) homodimers. Despite evidence attesting to the overall physiologic importance of Bcl-3, little is known about its cell-specific functions or mechanisms. Here we demonstrate a T cell-intrinsic function of Bcl-3 in autoimmunity. Bcl-3-deficient T cells failed to induce disease in T cell transfer-induced colitis and experimental autoimmune encephalomyelitis. The protection against disease correlated with a decrease in Th1 cells that produced the cytokines IFN?- and GM-CSF, and an increase in Th17 cells. Although differentiation into Th1 cells was not impaired in the absence of Bcl-3, differentiated Th1 cells converted to less pathogenic Th17-like cells, in part via mechanisms involving expression of the ROR?t transcription factor. Thus, Bcl-3 constrained Th1 cell plasticity and promoted pathogenicity by blocking conversion to Th17-like cells, revealing a unique type of regulation that shapes adaptive immunity. äThe oncoprotein and transcriptional regulator Bcl-3 governs plasticity(epmc).pdf DeepDyve Pubget Overpricing