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10.1126/sciimmunol.aai7616 http://scihub22266oqcxt.onion/10.1126/sciimmunol.aai7616 C5447456!5447456!28567448     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Sci+Immunol 2017 ; 2 (10): ä Nephropedia Template TP {{tp|p=28567448|t=2017. Type I Interferon Responses Drive Intrahepatic T cells to Promote Metabolic Syndrome |pdf=|usr=}}{{28567448}} gab.com Text Type I Interferon Responses Drive Intrahepatic T cells to Promote Metabolic Syndrome JO: Sci Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28567448 #FOAvip Obesity-related insulin resistance is driven by low-grade chronic inflammation of metabolic tissues. In the liver, non-alcoholic fatty liver disease (NAFLD) is associated with hepatic insulin resistance and systemic glucose dysregulation. However, the immunological factors supporting these processes are poorly understood. We found that the liver accumulates pathogenic CD8+ T cell subsets which control hepatic insulin sensitivity and gluconeogenesis during diet-induced obesity in mice. In a cohort of human patients, CD8+ T cells represent a dominant intrahepatic immune cell population which links to glucose dysregulation. Accumulation and activation of these cells are largely supported by type I interferon (IFN-I) responses in the liver. Livers from obese mice upregulate critical interferon regulatory factors (IRFs), interferon stimulatory genes (ISGs), and IFN? protein, while IFN?R1?/? mice, or CD8-specific IFN?R1?/? chimeric mice are protected from disease. IFN?R1 inhibitors improve metabolic parameters in mice, while CD8+ T cells and IFN-I responses correlate with NAFLD activity in human patients. Thus, IFN-I responses represent a central immunological axis that governs intrahepatic T cell pathogenicity during metabolic disease. Twit Text FOAVip Type I Interferon Responses Drive Intrahepatic T cells to Promote Metabolic Syndrome ????Sci Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28567448 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28567448 #FOAvip English Wikipedia <ref>{{Cite pmid|28567448}}</ref> Type I Interferon Responses Drive Intrahepatic T cells to Promote Metabolic Syndrome #MMPMID28567448 Ghazarian M; Revelo XS; Nøhr MK; Luck H; Zeng K; Lei H; Tsai S; Schroer SA; Park YJ; Chng MHY; Shen L; D?Angelo JA; Horton P; Chapman WC; Brockmeier D; Woo M; Engleman EG; Adeyi O; Hirano N; Jin T; Gehring AJ; Winer S; Winer DA Sci Immunol 2017[Apr]; 2 (10): ä PMID28567448show ga Obesity-related insulin resistance is driven by low-grade chronic inflammation of metabolic tissues. In the liver, non-alcoholic fatty liver disease (NAFLD) is associated with hepatic insulin resistance and systemic glucose dysregulation. However, the immunological factors supporting these processes are poorly understood. We found that the liver accumulates pathogenic CD8+ T cell subsets which control hepatic insulin sensitivity and gluconeogenesis during diet-induced obesity in mice. In a cohort of human patients, CD8+ T cells represent a dominant intrahepatic immune cell population which links to glucose dysregulation. Accumulation and activation of these cells are largely supported by type I interferon (IFN-I) responses in the liver. Livers from obese mice upregulate critical interferon regulatory factors (IRFs), interferon stimulatory genes (ISGs), and IFN? protein, while IFN?R1?/? mice, or CD8-specific IFN?R1?/? chimeric mice are protected from disease. IFN?R1 inhibitors improve metabolic parameters in mice, while CD8+ T cells and IFN-I responses correlate with NAFLD activity in human patients. Thus, IFN-I responses represent a central immunological axis that governs intrahepatic T cell pathogenicity during metabolic disease. äType I Interferon Responses Drive Intrahepatic T cells to Promote Meta(epmc).pdf DeepDyve Pubget Overpricing