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10.4049/jimmunol.2000554 http://scihub22266oqcxt.onion/10.4049/jimmunol.2000554 32651218!7486691!32651218     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       J+Immunol 2020 ; 205 (4): 892-898 Nephropedia Template TP {{tp|p=32651218|t=2020. A Case for Targeting Th17 Cells and IL-17A in SARS-CoV-2 Infections |pdf=|usr=}}{{32651218}} gab.com Text A Case for Targeting Th17 Cells and IL-17A in SARS-CoV-2 Infections JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=32651218 #FOAvip SARS-CoV-2, the virus causing COVID-19, has infected millions and has caused hundreds of thousands of fatalities. Risk factors for critical illness from SARS-CoV-2 infection include male gender, obesity, diabetes, and age >65. The mechanisms underlying the susceptibility to critical illness are poorly understood. Of interest, these comorbidities have previously been associated with increased signaling of Th17 cells. Th17 cells secrete IL-17A and are important for clearing extracellular pathogens, but inappropriate signaling has been linked to acute respiratory distress syndrome. Currently there are few treatment options for SARS-CoV-2 infections. This review describes evidence linking risk factors for critical illness in COVID-19 with increased Th17 cell activation and IL-17 signaling that may lead to increased likelihood for lung injury and respiratory failure. These findings provide a basis for testing the potential use of therapies directed at modulation of Th17 cells and IL-17A signaling in the treatment of COVID-19. Twit Text FOAVip A Case for Targeting Th17 Cells and IL-17A in SARS-CoV-2 Infections ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=32651218 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32651218 #FOAvip English Wikipedia <ref>{{Cite pmid|32651218}}</ref> A Case for Targeting Th17 Cells and IL-17A in SARS-CoV-2 Infections #MMPMID32651218 Orlov M; Wander PL; Morrell ED; Mikacenic C; Wurfel MM J Immunol 2020[Aug]; 205 (4): 892-898 PMID32651218show ga SARS-CoV-2, the virus causing COVID-19, has infected millions and has caused hundreds of thousands of fatalities. Risk factors for critical illness from SARS-CoV-2 infection include male gender, obesity, diabetes, and age >65. The mechanisms underlying the susceptibility to critical illness are poorly understood. Of interest, these comorbidities have previously been associated with increased signaling of Th17 cells. Th17 cells secrete IL-17A and are important for clearing extracellular pathogens, but inappropriate signaling has been linked to acute respiratory distress syndrome. Currently there are few treatment options for SARS-CoV-2 infections. This review describes evidence linking risk factors for critical illness in COVID-19 with increased Th17 cell activation and IL-17 signaling that may lead to increased likelihood for lung injury and respiratory failure. These findings provide a basis for testing the potential use of therapies directed at modulation of Th17 cells and IL-17A signaling in the treatment of COVID-19. |Antibodies, Monoclonal, Humanized/adverse effects/*therapeutic use[MESH] |Betacoronavirus/*immunology[MESH] |COVID-19[MESH] |COVID-19 Drug Treatment[MESH] |Comorbidity[MESH] |Coronavirus Infections/drug therapy/*epidemiology/*immunology/virology[MESH] |Critical Illness[MESH] |Female[MESH] |Humans[MESH] |Interleukin-17/*antagonists & inhibitors/metabolism[MESH] |Male[MESH] |Pandemics[MESH] |Pneumonia, Viral/*epidemiology/*immunology/virology[MESH] |Respiratory Distress Syndrome/immunology/mortality/virology[MESH] |Risk Factors[MESH] |SARS-CoV-2[MESH] |Signal Transduction/drug effects/immunology[MESH]A Case for Targeting Th17 Cells and IL-17A in SARS-CoV-2 Infections (epmc).pdf DeepDyve Pubget Overpricing