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10.1038/ncomms7131 http://scihub22266oqcxt.onion/10.1038/ncomms7131 C4302761!4302761!25607885     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 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 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2015 ; 6 (ä): 6131 Nephropedia Template TP {{tp|p=25607885|t=2015. IL-10 engages macrophages to shift Th17 cytokine dependency and pathogenicity during T cell-mediated colitis |pdf=|usr=}}{{25607885}} gab.com Text IL-10 engages macrophages to shift Th17 cytokine dependency and pathogenicity during T cell-mediated colitis JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=25607885 #FOAvip Polymorphisms attenuating IL-10 signaling confer genetic risk for inflammatory bowel disease. Yet how IL-10 prevents mucosal autoinflammation is incompletely understood. We demonstrate using lineage-specific deletions of IL-10R? that IL-10 acts primarily through macrophages to limit colitis. Colitis depends on IL-6 to support pathologic Th17 cell generation in wild type mice. However, specific ablation of macrophage IL-10R? provokes excessive IL-1? production that overrides Th17 IL-6 dependence, amplifying the colonic Th17 response and disease severity. IL-10 not only inhibits pro-IL-1? production transcriptionally in macrophages, but suppresses caspase-1 activation and caspase-1 dependent maturation of pro-IL-1? to IL-1?. Therefore lineage-specific effects of IL-10 skew the cytokine dependency of Th17 development required for colitis pathogenesis. Coordinated interventions may be needed to fully suppress Th17-mediated immunopathology. Twit Text FOAVip IL-10 engages macrophages to shift Th17 cytokine dependency and pathogenicity during T cell-mediated colitis ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=25607885 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25607885 #FOAvip English Wikipedia <ref>{{Cite pmid|25607885}}</ref> IL-10 engages macrophages to shift Th17 cytokine dependency and pathogenicity during T cell-mediated colitis #MMPMID25607885 Li B; Gurung P; Subbarao Malireddi RK; Vogel P; Kanneganti TD; Geiger TL Nat Commun 2015[]; 6 (ä): 6131 PMID25607885show ga Polymorphisms attenuating IL-10 signaling confer genetic risk for inflammatory bowel disease. Yet how IL-10 prevents mucosal autoinflammation is incompletely understood. We demonstrate using lineage-specific deletions of IL-10R? that IL-10 acts primarily through macrophages to limit colitis. Colitis depends on IL-6 to support pathologic Th17 cell generation in wild type mice. However, specific ablation of macrophage IL-10R? provokes excessive IL-1? production that overrides Th17 IL-6 dependence, amplifying the colonic Th17 response and disease severity. IL-10 not only inhibits pro-IL-1? production transcriptionally in macrophages, but suppresses caspase-1 activation and caspase-1 dependent maturation of pro-IL-1? to IL-1?. Therefore lineage-specific effects of IL-10 skew the cytokine dependency of Th17 development required for colitis pathogenesis. Coordinated interventions may be needed to fully suppress Th17-mediated immunopathology. äIL-10 engages macrophages to shift Th17 cytokine dependency and pathog(epmc).pdf DeepDyve Pubget Overpricing