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. 2022 May 16;39(9):110904. doi: 10.1016/j.celrep.2022.110904

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© 2022 The Author(s)

Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

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FcγR activation correlates with COVID-19 severity and anti-spike titers

The figure depicts the levels of FcγR-signaling induced by purified IgG from CoV-2⁺ donors in response to SARS-CoV-2 spike protein expressed on the surface of 293T cells.

(A–D) Graphs show the levels of (A and B) FcγRIIa and (C and D) FcγRIIIa signaling using 25 μg/mL IgG by (B and D) composite symptom severity scores or by (A and C) CoV−/+ status and severity scores.

(E–H) The panels compare the anti-spike IgG titers as quantified by CBA or ELISA assays versus the levels of FcγR signaling. (E and F) CBA anti-spike IgG versus (E) FcγRIIa and (F) FcγRIIIa signaling using 25 μg/mL IgG. (G and H) ELISA anti-spike IgG titers versus (G) FcγRIIa and (H) FcγRIIIa signaling using 25 μg/mL IgG. All of the FcγR results are the SEMs of N = 3 experiments.