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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 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 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 autoimmune T cells |pdf=|usr=}}{{25367572 }} gab.com Text The oncoprotein and transcriptional regulator Bcl-3 governs plasticity and pathogenicity of autoimmune 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 autoimmune 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 autoimmune T cells #MMPMID25367572 Tang W ; Wang H ; Claudio E ; Tassi I ; Ha HL ; Saret S ; Siebenlist U Immunity 2014[Oct]; 41 (4 ): 555-66 PMID25367572 show 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. |Animals [MESH] |Autoimmunity/*immunology [MESH] |B-Cell Lymphoma 3 Protein [MESH] |Cell Differentiation/immunology [MESH] |Colitis/immunology [MESH] |Encephalomyelitis, Autoimmune, Experimental/*immunology [MESH] |Granulocyte-Macrophage Colony-Stimulating Factor/*biosynthesis [MESH] |Homeodomain Proteins/genetics [MESH] |Interferon-gamma/*biosynthesis [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |NF-kappa B p50 Subunit/immunology [MESH] |NF-kappa B p52 Subunit/immunology [MESH] |Nuclear Receptor Subfamily 1, Group F, Member 3/biosynthesis/immunology [MESH] |Proto-Oncogene Proteins/genetics/*immunology [MESH] |Th1 Cells/*immunology/transplantation [MESH] |Th17 Cells/*immunology [MESH]The oncoprotein and transcriptional regulator Bcl-3 governs plasticity(epmc).pdf DeepDyve Pubget Overpricing