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10.1093/oxfimm/iqaa005 http://scihub22266oqcxt.onion/10.1093/oxfimm/iqaa005 34192268!7798612!34192268     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oxf+Open+Immunol 2020 ; 1 (1): iqaa005 Nephropedia Template TP {{tp|p=34192268|t=2020. Innate immunology in COVID-19-a living review Part II: dysregulated inflammation drives immunopathology |pdf=|usr=}}{{34192268}} gab.com Text Innate immunology in COVID-19-a living review Part II: dysregulated inflammation drives immunopathology JO: Oxf Open Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34192268 #FOAvip The current pandemic of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) poses a global health crisis and will likely continue to impact public health for years. As the effectiveness of the innate immune response is crucial to patient outcome, huge efforts have been made to understand how dysregulated immune responses may contribute to disease progression. Here we have reviewed current knowledge of cellular innate immune responses to SARS-CoV-2 infection, highlighting areas for further investigation and suggesting potential strategies for intervention. We conclude that in severe COVID-19 initial innate responses, primarily type I interferon, are suppressed or sabotaged which results in an early interleukin (IL)-6, IL-10 and IL-1beta-enhanced hyperinflammation. This inflammatory environment is driven by aberrant function of innate immune cells: monocytes, macrophages and natural killer cells dispersing viral pathogen-associated molecular patterns and damage-associated molecular patterns into tissues. This results in primarily neutrophil-driven pathology including fibrosis that causes acute respiratory distress syndrome. Activated leukocytes and neutrophil extracellular traps also promote immunothrombotic clots that embed into the lungs and kidneys of severe COVID-19 patients, are worsened by immobility in the intensive care unit and are perhaps responsible for the high mortality. Therefore, treatments that target inflammation and coagulation are promising strategies for reducing mortality in COVID-19. Twit Text FOAVip Innate immunology in COVID-19-a living review Part II: dysregulated inflammation drives immunopathology ????Oxf Open Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34192268 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34192268 #FOAvip English Wikipedia <ref>{{Cite pmid|34192268}}</ref> Innate immunology in COVID-19-a living review Part II: dysregulated inflammation drives immunopathology #MMPMID34192268 Rodrigues PRS; Alrubayyi A; Pring E; Bart VMT; Jones R; Coveney C; Lu F; Tellier M; Maleki-Toyserkani S; Richter FC; Scourfield DO; Gea-Mallorqui E; Davies LC Oxf Open Immunol 2020[]; 1 (1): iqaa005 PMID34192268show ga The current pandemic of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) poses a global health crisis and will likely continue to impact public health for years. As the effectiveness of the innate immune response is crucial to patient outcome, huge efforts have been made to understand how dysregulated immune responses may contribute to disease progression. Here we have reviewed current knowledge of cellular innate immune responses to SARS-CoV-2 infection, highlighting areas for further investigation and suggesting potential strategies for intervention. We conclude that in severe COVID-19 initial innate responses, primarily type I interferon, are suppressed or sabotaged which results in an early interleukin (IL)-6, IL-10 and IL-1beta-enhanced hyperinflammation. This inflammatory environment is driven by aberrant function of innate immune cells: monocytes, macrophages and natural killer cells dispersing viral pathogen-associated molecular patterns and damage-associated molecular patterns into tissues. This results in primarily neutrophil-driven pathology including fibrosis that causes acute respiratory distress syndrome. Activated leukocytes and neutrophil extracellular traps also promote immunothrombotic clots that embed into the lungs and kidneys of severe COVID-19 patients, are worsened by immobility in the intensive care unit and are perhaps responsible for the high mortality. Therefore, treatments that target inflammation and coagulation are promising strategies for reducing mortality in COVID-19. äInnate immunology in COVID-19-a living review Part II: dysregulated i(epmc).pdf DeepDyve Pubget Overpricing