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10.4049/jimmunol.2001407 http://scihub22266oqcxt.onion/10.4049/jimmunol.2001407 34078711!8278276!34078711     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       J+Immunol 2021 ; 206 (12): 3000-3009 Nephropedia Template TP {{tp|p=34078711|t=2021. Surface Proteins of SARS-CoV-2 Drive Airway Epithelial Cells to Induce IFN-Dependent Inflammation |pdf=|usr=}}{{34078711}} gab.com Text Surface Proteins of SARS-CoV-2 Drive Airway Epithelial Cells to Induce IFN-Dependent Inflammation JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34078711 #FOAvip SARS-CoV-2, the virus that has caused the COVID-19 pandemic, robustly activates the host immune system in critically ill patients. Understanding how the virus engages the immune system will facilitate the development of needed therapeutic strategies. In this study, we demonstrate both in vitro and in vivo that the SARS-CoV-2 surface proteins spike (S) and envelope (E) activate the key immune signaling IFN pathway in both human and mouse immune and epithelial cells independent of viral infection and replication. These proteins induce reactive oxidative species generation and increases in human- and murine-specific, IFN-responsive cytokines and chemokines, similar to their upregulation in critically ill COVID-19 patients. Induction of IFN signaling is dependent on canonical but discrepant inflammatory signaling mediators, as the activation induced by S is dependent on IRF3, TBK1, and MyD88, whereas that of E is largely MyD88 independent. Furthermore, these viral surface proteins, specifically E, induced peribronchial inflammation and pulmonary vasculitis in a mouse model. Finally, we show that the organized inflammatory infiltrates are dependent on type I IFN signaling, specifically in lung epithelial cells. These findings underscore the role of SARS-CoV-2 surface proteins, particularly the understudied E protein, in driving cell specific inflammation and their potential for therapeutic intervention. Twit Text FOAVip Surface Proteins of SARS-CoV-2 Drive Airway Epithelial Cells to Induce IFN-Dependent Inflammation ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34078711 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34078711 #FOAvip English Wikipedia <ref>{{Cite pmid|34078711}}</ref> Surface Proteins of SARS-CoV-2 Drive Airway Epithelial Cells to Induce IFN-Dependent Inflammation #MMPMID34078711 Anand G; Perry AM; Cummings CL; St Raymond E; Clemens RA; Steed AL J Immunol 2021[Jun]; 206 (12): 3000-3009 PMID34078711show ga SARS-CoV-2, the virus that has caused the COVID-19 pandemic, robustly activates the host immune system in critically ill patients. Understanding how the virus engages the immune system will facilitate the development of needed therapeutic strategies. In this study, we demonstrate both in vitro and in vivo that the SARS-CoV-2 surface proteins spike (S) and envelope (E) activate the key immune signaling IFN pathway in both human and mouse immune and epithelial cells independent of viral infection and replication. These proteins induce reactive oxidative species generation and increases in human- and murine-specific, IFN-responsive cytokines and chemokines, similar to their upregulation in critically ill COVID-19 patients. Induction of IFN signaling is dependent on canonical but discrepant inflammatory signaling mediators, as the activation induced by S is dependent on IRF3, TBK1, and MyD88, whereas that of E is largely MyD88 independent. Furthermore, these viral surface proteins, specifically E, induced peribronchial inflammation and pulmonary vasculitis in a mouse model. Finally, we show that the organized inflammatory infiltrates are dependent on type I IFN signaling, specifically in lung epithelial cells. These findings underscore the role of SARS-CoV-2 surface proteins, particularly the understudied E protein, in driving cell specific inflammation and their potential for therapeutic intervention. |Animals[MESH] |Cell Line, Tumor[MESH] |Coronavirus Envelope Proteins/*immunology[MESH] |Epithelial Cells/*immunology/virology[MESH] |Female[MESH] |Humans[MESH] |Inflammation/*immunology[MESH] |Interferon Type I/*immunology[MESH] |Male[MESH] |Mice[MESH]Surface Proteins of SARS-CoV-2 Drive Airway Epithelial Cells to Induce(epmc).pdf DeepDyve Pubget Overpricing