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10.15252/emmm.201606413 http://scihub22266oqcxt.onion/10.15252/emmm.201606413 C5009813!5009813!27520969     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 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       EMBO+Mol+Med 2016 ; 8 (9): 1099-112 Nephropedia Template TP {{tp|p=27520969|t=2016. IFN? is a potent anti?influenza therapeutic without the inflammatory side effects of IFN? treatment |pdf=|usr=}}{{27520969}} gab.com Text IFN is a potent anti influenza therapeutic without the inflammatory side effects of IFN treatment JO: EMBO Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=27520969 #FOAvip Influenza A virus (IAV)?induced severe disease is characterized by infected lung epithelia, robust inflammatory responses and acute lung injury. Since type I interferon (IFN??) and type III interferon (IFN?) are potent antiviral cytokines with immunomodulatory potential, we assessed their efficacy as IAV treatments. IFN? treatment of IAV?infected Mx1?positive mice lowered viral load and protected from disease. IFN? treatment also restricted IAV replication but exacerbated disease. IFN? treatment increased pulmonary proinflammatory cytokine secretion, innate cell recruitment and epithelial cell death, unlike IFN??treatment. IFN? lacked the direct stimulatory activity of IFN? on immune cells. In epithelia, both IFNs induced antiviral genes but no inflammatory cytokines. Similarly, human airway epithelia responded to both IFN? and IFN? by induction of antiviral genes but not of cytokines, while hPBMCs responded only to IFN?. The restriction of both IFN? responsiveness and productive IAV replication to pulmonary epithelia allows IFN? to limit IAV spread through antiviral gene induction in relevant cells without overstimulating the immune system and driving immunopathology. We propose IFN? as a non?inflammatory and hence superior treatment option for human IAV infection. Twit Text FOAVip IFN is a potent anti influenza therapeutic without the inflammatory side effects of IFN treatment ????EMBO Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=27520969 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27520969 #FOAvip English Wikipedia <ref>{{Cite pmid|27520969}}</ref> IFN? is a potent anti?influenza therapeutic without the inflammatory side effects of IFN? treatment #MMPMID27520969 Davidson S; McCabe TM; Crotta S; Gad HH; Hessel EM; Beinke S; Hartmann R; Wack A EMBO Mol Med 2016[Sep]; 8 (9): 1099-112 PMID27520969show ga Influenza A virus (IAV)?induced severe disease is characterized by infected lung epithelia, robust inflammatory responses and acute lung injury. Since type I interferon (IFN??) and type III interferon (IFN?) are potent antiviral cytokines with immunomodulatory potential, we assessed their efficacy as IAV treatments. IFN? treatment of IAV?infected Mx1?positive mice lowered viral load and protected from disease. IFN? treatment also restricted IAV replication but exacerbated disease. IFN? treatment increased pulmonary proinflammatory cytokine secretion, innate cell recruitment and epithelial cell death, unlike IFN??treatment. IFN? lacked the direct stimulatory activity of IFN? on immune cells. In epithelia, both IFNs induced antiviral genes but no inflammatory cytokines. Similarly, human airway epithelia responded to both IFN? and IFN? by induction of antiviral genes but not of cytokines, while hPBMCs responded only to IFN?. The restriction of both IFN? responsiveness and productive IAV replication to pulmonary epithelia allows IFN? to limit IAV spread through antiviral gene induction in relevant cells without overstimulating the immune system and driving immunopathology. We propose IFN? as a non?inflammatory and hence superior treatment option for human IAV infection. äIFN? is a potent anti?influenza therapeutic without the inflammatory s(epmc).pdf DeepDyve Pubget Overpricing