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10.1172/jci.insight.140329

http://scihub22266oqcxt.onion/10.1172/jci.insight.140329
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32687484!7526441!32687484
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suck abstract from ncbi


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pmid32687484      JCI+Insight 2020 ; 5 (17): ä
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  • Severe immunosuppression and not a cytokine storm characterizes COVID-19 infections #MMPMID32687484
  • Remy KE; Mazer M; Striker DA; Ellebedy AH; Walton AH; Unsinger J; Blood TM; Mudd PA; Yi DJ; Mannion DA; Osborne DF; Martin RS; Anand NJ; Bosanquet JP; Blood J; Drewry AM; Caldwell CC; Turnbull IR; Brakenridge SC; Moldwawer LL; Hotchkiss RS
  • JCI Insight 2020[Sep]; 5 (17): ä PMID32687484show ga
  • COVID-19-associated morbidity and mortality have been attributed to a pathologic host response. Two divergent hypotheses have been proposed: hyperinflammatory cytokine storm; and failure of host protective immunity that results in unrestrained viral dissemination and organ injury. A key explanation for the inability to address this controversy has been the lack of diagnostic tools to evaluate immune function in COVID-19 infections. ELISpot, a highly sensitive, functional immunoassay, was employed in 27 patients with COVID-19, 51 patients with sepsis, 18 critically ill nonseptic (CINS) patients, and 27 healthy control volunteers to evaluate adaptive and innate immune status by quantitating T cell IFN-? and monocyte TFN-alpha production. Circulating T cell subsets were profoundly reduced in COVID-19 patients. Additionally, stimulated blood mononuclear cells produced less than 40%-50% of the IFN-? and TNF-alpha observed in septic and CINS patients, consistent with markedly impaired immune effector cell function. Approximately 25% of COVID-19 patients had increased IL-6 levels that were not associated with elevations in other canonical proinflammatory cytokines. Collectively, these findings support the hypothesis that COVID-19 suppresses host functional adaptive and innate immunity. Importantly, IL-7 administered ex vivo restored T cell IFN-? production in COVID-19 patients. Thus, ELISpot may functionally characterize host immunity in COVID-19 and inform prospective therapies.
  • |Adaptive Immunity/*immunology[MESH]
  • |Adolescent[MESH]
  • |Adult[MESH]
  • |Aged[MESH]
  • |Aged, 80 and over[MESH]
  • |Betacoronavirus[MESH]
  • |COVID-19[MESH]
  • |Case-Control Studies[MESH]
  • |Coronavirus Infections/*immunology[MESH]
  • |Critical Illness[MESH]
  • |Cytokine Release Syndrome/*immunology[MESH]
  • |Enzyme-Linked Immunospot Assay[MESH]
  • |Female[MESH]
  • |Healthy Volunteers[MESH]
  • |Humans[MESH]
  • |Immune Tolerance/*immunology[MESH]
  • |Immunity, Innate/*immunology[MESH]
  • |Interferon-gamma/immunology/metabolism[MESH]
  • |Interleukin-6/immunology[MESH]
  • |Male[MESH]
  • |Middle Aged[MESH]
  • |Monocytes/immunology/metabolism[MESH]
  • |Pandemics[MESH]
  • |Pneumonia, Viral/*immunology[MESH]
  • |SARS-CoV-2[MESH]
  • |Sepsis/*immunology[MESH]
  • |T-Lymphocyte Subsets/immunology/metabolism[MESH]
  • |T-Lymphocytes/immunology/metabolism[MESH]
  • |Tumor Necrosis Factor-alpha/immunology/metabolism[MESH]


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