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10.1038/mi.2017.41 http://scihub22266oqcxt.onion/10.1038/mi.2017.41 C5693789!5693789!28513592     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 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       Mucosal+Immunol 2018 ; 11 (1): 209-19 Nephropedia Template TP {{tp|p=28513592|t=2018. IFN-? increases susceptibility to influenza A infection through suppression of group II innate lymphoid cells |pdf=|usr=}}{{28513592}} gab.com Text IFN- increases susceptibility to influenza A infection through suppression of group II innate lymphoid cells JO: Mucosal Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28513592 #FOAvip Increased levels of IFN-? are routinely observed in the respiratory tract following influenza virus infection, yet its potential role remains unclear. We now demonstrate that influenza-induced IFN-? restricts protective innate lymphoid cell group II (ILC2) function in the lung following challenge with the pandemic H1N1 A/CA/04/2009 influenza virus. Specifically, IFN-? deficiency resulted in enhanced ILC2 activity, characterized by increased production of IL-5 and amphiregulin, and improved tissue integrity, yet no change in ILC2 numbers, viral load or clearance. We further found that IFN-?-deficient mice, as well as wild-type animals treated with neutralizing anti-IFN-? antibody, exhibited decreased susceptibility to lethal infection with H1N1 A/CA/04/2009 influenza virus, and moreover that survival was dependent on the presence of IL-5. The beneficial effects of IFN-? neutralization were not observed in ILC2-deficient animals. These data support the novel concept that IFN-? can play a detrimental role in the pathogenesis of influenza through a restriction in ILC2 activity. Thus, regulation of ILC2 activity is a potential target for post-infection therapy of influenza. Twit Text FOAVip IFN- increases susceptibility to influenza A infection through suppression of group II innate lymphoid cells ????Mucosal Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28513592 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28513592 #FOAvip English Wikipedia <ref>{{Cite pmid|28513592}}</ref> IFN-? increases susceptibility to influenza A infection through suppression of group II innate lymphoid cells #MMPMID28513592 Califano D; Furuya Y; Roberts S; Avram D; McKenzie AN; Metzger DW Mucosal Immunol 2018[Jan]; 11 (1): 209-19 PMID28513592show ga Increased levels of IFN-? are routinely observed in the respiratory tract following influenza virus infection, yet its potential role remains unclear. We now demonstrate that influenza-induced IFN-? restricts protective innate lymphoid cell group II (ILC2) function in the lung following challenge with the pandemic H1N1 A/CA/04/2009 influenza virus. Specifically, IFN-? deficiency resulted in enhanced ILC2 activity, characterized by increased production of IL-5 and amphiregulin, and improved tissue integrity, yet no change in ILC2 numbers, viral load or clearance. We further found that IFN-?-deficient mice, as well as wild-type animals treated with neutralizing anti-IFN-? antibody, exhibited decreased susceptibility to lethal infection with H1N1 A/CA/04/2009 influenza virus, and moreover that survival was dependent on the presence of IL-5. The beneficial effects of IFN-? neutralization were not observed in ILC2-deficient animals. These data support the novel concept that IFN-? can play a detrimental role in the pathogenesis of influenza through a restriction in ILC2 activity. Thus, regulation of ILC2 activity is a potential target for post-infection therapy of influenza. äIFN-? increases susceptibility to influenza A infection through suppre(epmc).pdf DeepDyve Pubget Overpricing