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10.1111/cei.12905 http://scihub22266oqcxt.onion/10.1111/cei.12905 C5343349!5343349!27880975     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 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 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 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\27880975.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Clin+Exp+Immunol 2017 ; 188 (1): 63-78 Nephropedia Template TP {{tp|p=27880975|t=2017. ROR?t expression in Tregs promotes systemic lupus erythematosus via IL?17 secretion, alteration of Treg phenotype and suppression of Th2 responses |pdf=|usr=}}{{27880975}} gab.com Text ROR t expression in Tregs promotes systemic lupus erythematosus via IL 17 secretion, alteration of Treg phenotype and suppression of Th2 responses JO: Clin Exp Immunol http://www.kidney.de/pget.php?&tw=1&pmid=27880975 #FOAvip Systemic lupus erythematosus (SLE) is a common autoimmune disorder with a complex and poorly understood immunopathogenesis. However, a pathogenic role for the T helper type 17 (Th17) axis was demonstrated by many studies, while regulatory T cells (Tregs) were shown to mediate protection. Recently, we and others characterized a novel and independent T cell population expressing both the Treg characteristic transcription factor forkhead box protein 3 (FoxP3) and the Th17?defining retinoic acid receptor?related orphan nuclear receptor ?t (ROR?t). Studies in a model of acute glomerulonephritis unveiled potent regulatory, but also proinflammatory, functions of ROR?t+FoxP3+ Tregs. This bi?functional nature prompted us to suggest the name ?biTregs?. Importantly, the pathogenic biTreg effects were dependent upon expression of ROR?t. We thus aimed to evaluate the contribution of ROR?t+FoxP3+ biTregs to pristane?induced SLE and explored the therapeutic potential of interference with ROR?t activation. Our analyses revealed expansion of IL?17 producing biTregs in a distinctive time?course and organ?specific pattern, coincident with the development of autoimmunity and tissue injury. Importantly, specific ablation of ROR?t activation in endogenous biTregs resulted in significant amelioration of pristane?induced pulmonary vasculitis and lupus nephritis. As potential mechanisms underlying the observed protection, we found that secretion of IL?17 by biTregs was abrogated completely in FoxP3Cre × RORCfl/fl mice. Furthermore, Tregs showed a more activated phenotype after cell?specific inactivation of ROR?t signalling. Finally, and remarkably, biTregs were found to potently suppress anti?inflammatory Th2 immunity in a ROR?t?dependent manner. Our study thus identifies biTregs as novel players in SLE and advocates ROR?t?directed interventions as promising therapeutic strategies. Twit Text FOAVip ROR t expression in Tregs promotes systemic lupus erythematosus via IL 17 secretion, alteration of Treg phenotype and suppression of Th2 responses ????Clin Exp Immunol http://www.kidney.de/pget.php?&tw=1&pmid=27880975 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27880975 #FOAvip English Wikipedia <ref>{{Cite pmid|27880975}}</ref> ROR?t expression in Tregs promotes systemic lupus erythematosus via IL?17 secretion, alteration of Treg phenotype and suppression of Th2 responses #MMPMID27880975 Kluger MA; Nosko A; Ramcke T; Goerke B; Meyer MC; Wegscheid C; Luig M; Tiegs G; Stahl RAK; Steinmetz OM Clin Exp Immunol 2017[Apr]; 188 (1): 63-78 PMID27880975show ga Systemic lupus erythematosus (SLE) is a common autoimmune disorder with a complex and poorly understood immunopathogenesis. However, a pathogenic role for the T helper type 17 (Th17) axis was demonstrated by many studies, while regulatory T cells (Tregs) were shown to mediate protection. Recently, we and others characterized a novel and independent T cell population expressing both the Treg characteristic transcription factor forkhead box protein 3 (FoxP3) and the Th17?defining retinoic acid receptor?related orphan nuclear receptor ?t (ROR?t). Studies in a model of acute glomerulonephritis unveiled potent regulatory, but also proinflammatory, functions of ROR?t+FoxP3+ Tregs. This bi?functional nature prompted us to suggest the name ?biTregs?. Importantly, the pathogenic biTreg effects were dependent upon expression of ROR?t. We thus aimed to evaluate the contribution of ROR?t+FoxP3+ biTregs to pristane?induced SLE and explored the therapeutic potential of interference with ROR?t activation. Our analyses revealed expansion of IL?17 producing biTregs in a distinctive time?course and organ?specific pattern, coincident with the development of autoimmunity and tissue injury. Importantly, specific ablation of ROR?t activation in endogenous biTregs resulted in significant amelioration of pristane?induced pulmonary vasculitis and lupus nephritis. As potential mechanisms underlying the observed protection, we found that secretion of IL?17 by biTregs was abrogated completely in FoxP3Cre × RORCfl/fl mice. Furthermore, Tregs showed a more activated phenotype after cell?specific inactivation of ROR?t signalling. Finally, and remarkably, biTregs were found to potently suppress anti?inflammatory Th2 immunity in a ROR?t?dependent manner. Our study thus identifies biTregs as novel players in SLE and advocates ROR?t?directed interventions as promising therapeutic strategies. äROR?t expression in Tregs promotes systemic lupus erythematosus via IL(epmc).pdf DeepDyve Pubget Overpricing