Fig. 5: FcγR2B⁺3B⁻- and FcγR2B⁻3B⁺-binding IgG show different abilities to drive antibody-dependent effector functions as well as cytokine and chemokine production.

a, The selection strategy of COVID-19⁺FcR2B⁺3B⁻ and COVID-19⁻FcR2B⁻3B⁺ pools based on the ability of WT S-specific IgG to bind to FcγR2B and FcγR3B receptors. Subjects in the top quartile (marked with boxes) were selected and pooled (pool of n = 5). b, ADCD. c,d, ADCP (c) and ADNP (d) in COVID-19⁺FcR2B⁺3B⁻ and COVID-19⁻FcR2B⁻3B⁺ pools (pool of n = 5). Bars show the mean value with s.d. Dots represents replicates (n = 4 and n = 6). Samples were run in technical duplicates and two (ADCD) to three (ADCP and ADNP) biological replicates. Unpaired Student’s t-test and P_adj (^***P < 0.001; ^**P < 0.01; ^*P < 0.05) were used. e, Cytokine production by isolated human neutrophils stimulated with COVID-19⁺FcR2B⁺3B⁻ and COVID-19⁻FcR2B⁻3B⁺ pools (pool of n = 5). Bars show the mean with s.d. Dots represent replicates (n = 4, technical duplicates of two biological replicates with different blood donors). Unpaired Student’s t-test and P_adj (^***P < 0.001; ^**P < 0.01; ^*P < 0.05) were used. GM-CSF, granulocyte–macrophage colony-stimulating factor; IFNγ, interferon-γ; MCP, monocyte chemoattractant protein; MIP, macrophage inflammatory protein; TGFα; transforming growth factor α; TNF-α, tumor necrosis factor α; VEGF, vascular endothelial growth factor.

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