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10.1038/mi.2017.41 http://scihub22266oqcxt.onion/10.1038/mi.2017.41 C5693789!5693789 !28513592     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28513592 &cmd=llinks): Failed to open stream: HTTP request failed! 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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 interferon-? (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 (CA04) influenza virus. Specifically, IFN-? deficiency resulted in enhanced ILC2 activity, characterized by increased production of interleukin (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 CA04 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 have 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 ANJ ; Metzger DW Mucosal Immunol 2018[Jan]; 11 (1 ): 209-219 PMID28513592 show ga Increased levels of interferon-? (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 (CA04) influenza virus. Specifically, IFN-? deficiency resulted in enhanced ILC2 activity, characterized by increased production of interleukin (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 CA04 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 have 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. |Animals [MESH] |Antibodies, Blocking/metabolism [MESH] |Cells, Cultured [MESH] |Disease Susceptibility [MESH] |Immunity, Innate [MESH] |Immunosuppression Therapy [MESH] |Influenza A Virus, H1N1 Subtype/*immunology [MESH] |Interferon-gamma/genetics/*metabolism [MESH] |Interleukin-5/*metabolism [MESH] |Lymphocytes/*immunology [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Orthomyxoviridae Infections/*immunology [MESH]IFN-? increases susceptibility to influenza A infection through suppre(epmc).pdf DeepDyve Pubget Overpricing