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10.4049/jimmunol.1501881 http://scihub22266oqcxt.onion/10.4049/jimmunol.1501881 C4761460!4761460!26826241     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Immunol 2016 ; 196 (5): 2283-92 Nephropedia Template TP {{tp|p=26826241|t=2016. Hepatitis C virus-induced MDSCs Suppress NK Cell Interferon-gamma Production by Altering Cellular Metabolism via Arginase-1 |pdf=|usr=}}{{26826241}} gab.com Text Hepatitis C virus-induced MDSCs Suppress NK Cell Interferon-gamma Production by Altering Cellular Metabolism via Arginase-1 JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26826241 #FOAvip The hepatitis C virus (HCV) infects ~200 million people worldwide. The majority of infected individuals develop persistent infection, resulting in chronic inflammation and liver disease, including cirrhosis and hepatocellular carcinoma. HCV?s ability to establish persistent infection is partly due to its ability to evade the immune response through multiple mechanisms, including suppression of natural killer (NK) cells. NK cells control HCV replication during the early phase of infection and regulate the progression to chronic disease. In particular, IFN-? produced by NK cells limits viral replication in hepatocytes and is important for the initiation of adaptive immune responses. However, NK cell function is significantly impaired in chronic HCV patients. The cellular and molecular mechanisms responsible for impaired NK cell function in HCV infection are not well defined. Here, we analyzed the interaction of human NK cells with CD33+ PBMCs that were exposed to HCV. We found that NK cells co-cultured with HCV-conditioned CD33+ PBMCs produced lower amounts of IFN-?, with no effect on granzyme B production or cell viability. Importantly, this suppression of NK cell-derived IFN-? production was mediated by CD33+CD11bloHLA-DRlo myeloid derived suppressor cells (MDSCs) via an arginase-1-dependent inhibition of mTOR activation. Suppression of IFN-? production was reversed by L-arginine supplementation, consistent with increased MDSC arginase-1 activity. These novel results identify the induction of MDSCs in HCV infection as a potent immune evasion strategy that suppresses anti-viral NK cell responses, further indicating that blockade of MDSCs may be a potential therapeutic approach to ameliorate chronic viral infections in the liver. Twit Text FOAVip Hepatitis C virus-induced MDSCs Suppress NK Cell Interferon-gamma Production by Altering Cellular Metabolism via Arginase-1 ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26826241 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26826241 #FOAvip English Wikipedia <ref>{{Cite pmid|26826241}}</ref> Hepatitis C virus-induced MDSCs Suppress NK Cell Interferon-gamma Production by Altering Cellular Metabolism via Arginase-1 #MMPMID26826241 Goh CC; Roggerson KM; Lee HC; Golden-Mason L; Rosen HR; Hahn YS J Immunol 2016[Mar]; 196 (5): 2283-92 PMID26826241show ga The hepatitis C virus (HCV) infects ~200 million people worldwide. The majority of infected individuals develop persistent infection, resulting in chronic inflammation and liver disease, including cirrhosis and hepatocellular carcinoma. HCV?s ability to establish persistent infection is partly due to its ability to evade the immune response through multiple mechanisms, including suppression of natural killer (NK) cells. NK cells control HCV replication during the early phase of infection and regulate the progression to chronic disease. In particular, IFN-? produced by NK cells limits viral replication in hepatocytes and is important for the initiation of adaptive immune responses. However, NK cell function is significantly impaired in chronic HCV patients. The cellular and molecular mechanisms responsible for impaired NK cell function in HCV infection are not well defined. Here, we analyzed the interaction of human NK cells with CD33+ PBMCs that were exposed to HCV. We found that NK cells co-cultured with HCV-conditioned CD33+ PBMCs produced lower amounts of IFN-?, with no effect on granzyme B production or cell viability. Importantly, this suppression of NK cell-derived IFN-? production was mediated by CD33+CD11bloHLA-DRlo myeloid derived suppressor cells (MDSCs) via an arginase-1-dependent inhibition of mTOR activation. Suppression of IFN-? production was reversed by L-arginine supplementation, consistent with increased MDSC arginase-1 activity. These novel results identify the induction of MDSCs in HCV infection as a potent immune evasion strategy that suppresses anti-viral NK cell responses, further indicating that blockade of MDSCs may be a potential therapeutic approach to ameliorate chronic viral infections in the liver. äHepatitis C virus-induced MDSCs Suppress NK Cell Interferon-gamma Prod(epmc).pdf DeepDyve Pubget Overpricing