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Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Cell+Rep+Med 2021 ; 2 (3): 100208 Nephropedia Template TP
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Integrated immune dynamics define correlates of COVID-19 severity and antibody responses #MMPMID33564749
Koutsakos M; Rowntree LC; Hensen L; Chua BY; van de Sandt CE; Habel JR; Zhang W; Jia X; Kedzierski L; Ashhurst TM; Putri GH; Marsh-Wakefield F; Read MN; Edwards DN; Clemens EB; Wong CY; Mordant FL; Juno JA; Amanat F; Audsley J; Holmes NE; Gordon CL; Smibert OC; Trubiano JA; Hughes CM; Catton M; Denholm JT; Tong SYC; Doolan DL; Kotsimbos TC; Jackson DC; Krammer F; Godfrey DI; Chung AW; King NJC; Lewin SR; Wheatley AK; Kent SJ; Subbarao K; McMahon J; Thevarajan I; Nguyen THO; Cheng AC; Kedzierska K
Cell Rep Med 2021[Mar]; 2 (3): 100208 PMID33564749show ga
SARS-CoV-2 causes a spectrum of COVID-19 disease, the immunological basis of which remains ill defined. We analyzed 85 SARS-CoV-2-infected individuals at acute and/or convalescent time points, up to 102 days after symptom onset, quantifying 184 immunological parameters. Acute COVID-19 presented with high levels of IL-6, IL-18, and IL-10 and broad activation marked by the upregulation of CD38 on innate and adaptive lymphocytes and myeloid cells. Importantly, activated CXCR3(+)cT(FH)1 cells in acute COVID-19 significantly correlate with and predict antibody levels and their avidity at convalescence as well as acute neutralization activity. Strikingly, intensive care unit (ICU) patients with severe COVID-19 display higher levels of soluble IL-6, IL-6R, and IL-18, and hyperactivation of innate, adaptive, and myeloid compartments than patients with moderate disease. Our analyses provide a comprehensive map of longitudinal immunological responses in COVID-19 patients and integrate key cellular pathways of complex immune networks underpinning severe COVID-19, providing important insights into potential biomarkers and immunotherapies.