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10.1038/ni.3288 http://scihub22266oqcxt.onion/10.1038/ni.3288 C4618075!4618075!26437242     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Immunol 2015 ; 16 (11): 1162-73 Nephropedia Template TP {{tp|p=26437242|t=2015. Control of peripheral tolerance by regulatory T cell-intrinsic Notch signaling |pdf=|usr=}}{{26437242}} gab.com Text Control of peripheral tolerance by regulatory T cell-intrinsic Notch signaling JO: Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26437242 #FOAvip Notch receptors direct the differentiation of T helper (TH) cell subsets, but their influence on regulatory T (Treg) cell responses is obscure. We here report that lineage-specific deletion of components of the Notch pathway enhanced Treg cell-mediated suppression of TH1 responses, and protected against their TH1 skewing and apoptosis. Expression in Treg cells of gain of function transgene encoding Notch1 intracellular domain resulted in lymphoproliferation, exacerbated TH1 responses and autoimmunity. Cell-intrinsic canonical Notch signaling impaired Treg cell fitness, promoted the acquisition by Treg cells of a TH1 cell-like phenotype, whereas Rictor-dependent non-canonical Notch signaling activated the AKT-Foxo1 axis and impaired Foxp3 epigenetic stability. These findings establish a critical role for Notch signaling in controlling peripheral Treg cell functions. Twit Text FOAVip Control of peripheral tolerance by regulatory T cell-intrinsic Notch signaling ????Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26437242 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26437242 #FOAvip English Wikipedia <ref>{{Cite pmid|26437242}}</ref> Control of peripheral tolerance by regulatory T cell-intrinsic Notch signaling #MMPMID26437242 Charbonnier LM; Wang S; Georgiev P; Sefik E; Chatila TA Nat Immunol 2015[Nov]; 16 (11): 1162-73 PMID26437242show ga Notch receptors direct the differentiation of T helper (TH) cell subsets, but their influence on regulatory T (Treg) cell responses is obscure. We here report that lineage-specific deletion of components of the Notch pathway enhanced Treg cell-mediated suppression of TH1 responses, and protected against their TH1 skewing and apoptosis. Expression in Treg cells of gain of function transgene encoding Notch1 intracellular domain resulted in lymphoproliferation, exacerbated TH1 responses and autoimmunity. Cell-intrinsic canonical Notch signaling impaired Treg cell fitness, promoted the acquisition by Treg cells of a TH1 cell-like phenotype, whereas Rictor-dependent non-canonical Notch signaling activated the AKT-Foxo1 axis and impaired Foxp3 epigenetic stability. These findings establish a critical role for Notch signaling in controlling peripheral Treg cell functions. äControl of peripheral tolerance by regulatory T cell-intrinsic Notch s(epmc).pdf DeepDyve Pubget Overpricing