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10.1126/science.abc2061 http://scihub22266oqcxt.onion/10.1126/science.abc2061 32527928!7292500!32527928     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Science 2020 ; 369 (6504): 712-717 Nephropedia Template TP {{tp|p=32527928|t=2020. Type I and III interferons disrupt lung epithelial repair during recovery from viral infection |pdf=|usr=}}{{32527928}} gab.com Text Type I and III interferons disrupt lung epithelial repair during recovery from viral infection JO: Science http://www.kidney.de/pget.php?&tw=1&pmid=32527928 #FOAvip Excessive cytokine signaling frequently exacerbates lung tissue damage during respiratory viral infection. Type I (IFN-alpha and IFN-beta) and III (IFN-lambda) interferons are host-produced antiviral cytokines. Prolonged IFN-alpha and IFN-beta responses can lead to harmful proinflammatory effects, whereas IFN-lambda mainly signals in epithelia, thereby inducing localized antiviral immunity. In this work, we show that IFN signaling interferes with lung repair during influenza recovery in mice, with IFN-lambda driving these effects most potently. IFN-induced protein p53 directly reduces epithelial proliferation and differentiation, which increases disease severity and susceptibility to bacterial superinfections. Thus, excessive or prolonged IFN production aggravates viral infection by impairing lung epithelial regeneration. Timing and duration are therefore critical parameters of endogenous IFN action and should be considered carefully for IFN therapeutic strategies against viral infections such as influenza and coronavirus disease 2019 (COVID-19). Twit Text FOAVip Type I and III interferons disrupt lung epithelial repair during recovery from viral infection ????Science http://www.kidney.de/pget.php?&tw=1&pmid=32527928 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32527928 #FOAvip English Wikipedia <ref>{{Cite pmid|32527928}}</ref> Type I and III interferons disrupt lung epithelial repair during recovery from viral infection #MMPMID32527928 Major J; Crotta S; Llorian M; McCabe TM; Gad HH; Priestnall SL; Hartmann R; Wack A Science 2020[Aug]; 369 (6504): 712-717 PMID32527928show ga Excessive cytokine signaling frequently exacerbates lung tissue damage during respiratory viral infection. Type I (IFN-alpha and IFN-beta) and III (IFN-lambda) interferons are host-produced antiviral cytokines. Prolonged IFN-alpha and IFN-beta responses can lead to harmful proinflammatory effects, whereas IFN-lambda mainly signals in epithelia, thereby inducing localized antiviral immunity. In this work, we show that IFN signaling interferes with lung repair during influenza recovery in mice, with IFN-lambda driving these effects most potently. IFN-induced protein p53 directly reduces epithelial proliferation and differentiation, which increases disease severity and susceptibility to bacterial superinfections. Thus, excessive or prolonged IFN production aggravates viral infection by impairing lung epithelial regeneration. Timing and duration are therefore critical parameters of endogenous IFN action and should be considered carefully for IFN therapeutic strategies against viral infections such as influenza and coronavirus disease 2019 (COVID-19). |Alveolar Epithelial Cells/immunology/*pathology[MESH] |Animals[MESH] |Apoptosis[MESH] |Bronchoalveolar Lavage Fluid/immunology[MESH] |Cell Differentiation[MESH] |Cell Proliferation[MESH] |Cells, Cultured[MESH] |Cytokines/administration & dosage/immunology/*metabolism[MESH] |Female[MESH] |Influenza A Virus, H3N2 Subtype[MESH] |Interferon Lambda[MESH] |Interferon Type I/administration & dosage/*metabolism/pharmacology[MESH] |Interferon-alpha/administration & dosage/metabolism/pharmacology[MESH] |Interferon-beta/administration & dosage/metabolism/pharmacology[MESH] |Interferons/administration & dosage/*metabolism/pharmacology[MESH] |Lung/*pathology[MESH] |Male[MESH] |Mice[MESH] |Orthomyxoviridae Infections/*immunology/metabolism/*pathology[MESH] |Receptor, Interferon alpha-beta/genetics/metabolism[MESH] |Receptors, Interferon/genetics/metabolism[MESH] |Signal Transduction[MESH]Type I and III interferons disrupt lung epithelial repair during recov(epmc).pdf DeepDyve Pubget Overpricing