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10.1038/ncomms10857 http://scihub22266oqcxt.onion/10.1038/ncomms10857 C4782063!4782063!26936133     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2016 ; 7 (ä): ä Nephropedia Template TP {{tp|p=26936133|t=2016. Itk is required for Th9 differentiation via TCR-mediated induction of IL-2 and IRF4 |pdf=|usr=}}{{26936133}} gab.com Text Itk is required for Th9 differentiation via TCR-mediated induction of IL-2 and IRF4 JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=26936133 #FOAvip Th9 cells produce interleukin (IL)-9, a cytokine implicated in allergic asthma and autoimmunity. Here we show that Itk, a mediator of T cell receptor signalling required for Th2 immune responses and the development of asthma, is a positive regulator of Th9 differentiation. In a model of allergic lung disease, Itk-deficient mice show reduced pulmonary inflammation and IL-9 production by T cells and innate lymphoid type 2 cells (ILC2), despite normal early induction of ILC2s. In vitro, Itk?/? CD4+ T cells do not produce IL-9 and have reduced levels of IRF4 (Interferon Regulator Factor 4), a critical transcription factor for effector T cell function. Both IL-9 and IRF4 expression are rescued by either IL-2 or constitutively active STAT5, but not NFATc1. STAT5 binds the Irf4 promoter, demonstrating one mechanism by which IL-2 rescues weakly activated T cells. Itk inhibition also reduces IL-9 expression by human T cells, implicating ITK as a key regulator of Th9 induction. Twit Text FOAVip Itk is required for Th9 differentiation via TCR-mediated induction of IL-2 and IRF4 ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=26936133 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26936133 #FOAvip English Wikipedia <ref>{{Cite pmid|26936133}}</ref> Itk is required for Th9 differentiation via TCR-mediated induction of IL-2 and IRF4 #MMPMID26936133 Gomez-Rodriguez J; Meylan F; Handon R; Hayes ET; Anderson SM; Kirby MR; Siegel RM; Schwartzberg PL Nat Commun 2016[]; 7 (ä): ä PMID26936133show ga Th9 cells produce interleukin (IL)-9, a cytokine implicated in allergic asthma and autoimmunity. Here we show that Itk, a mediator of T cell receptor signalling required for Th2 immune responses and the development of asthma, is a positive regulator of Th9 differentiation. In a model of allergic lung disease, Itk-deficient mice show reduced pulmonary inflammation and IL-9 production by T cells and innate lymphoid type 2 cells (ILC2), despite normal early induction of ILC2s. In vitro, Itk?/? CD4+ T cells do not produce IL-9 and have reduced levels of IRF4 (Interferon Regulator Factor 4), a critical transcription factor for effector T cell function. Both IL-9 and IRF4 expression are rescued by either IL-2 or constitutively active STAT5, but not NFATc1. STAT5 binds the Irf4 promoter, demonstrating one mechanism by which IL-2 rescues weakly activated T cells. Itk inhibition also reduces IL-9 expression by human T cells, implicating ITK as a key regulator of Th9 induction. äItk is required for Th9 differentiation via TCR-mediated induction of (epmc).pdf DeepDyve Pubget Overpricing