Fig. 3: The immune response is dysregulated in severe COVID-19 patients.

a–h Plasma levels of IFNs and inflammatory cytokines in healthy controls, mild and severe COVID-19 patients were measured at two different timepoints after symptom onset (5–10 days and ≥10 days after symptom onset). Box plots display the median (center line), interquartile range (box bounds), and 1.5 times the interquartile range (whiskers). i PBMCs from 11 healthy controls and 14 COVID-19 patients (at an early infection phase, i.e., <10 days since symptom onset) were collected, and T and B cells were depleted. UMAP representation of all merged scRNA-seq profiles are shown. 13 cell types were identified by cluster gene signatures. j Violin plots showing top marker genes for the cell types shown in (i). k Relative abundance of major innate immune cells were compared. Their distribution varies between controls and COVID-19 patients and between mild and severe disease. Significant pairwise comparisons are denoted in panels (a–h) and (k) (Mann–Whitney U test). See also Supplementary Figure 2. IFNα interferon alpha, IFNγ interferon gamma, IFNλ2 interferon lambda 2, IP-10 interferon gamma-induced protein 10, TNFα tumor necrosis factor alpha, IL-5 interleukin-5, CCL2 CC-chemokin-ligand-2, IL-10 interleukin-10, n.m. not measured; scRNAseq single-cell RNA sequencing, PBMCs peripheral mononuclear blood cells, cMono classical monocytes, ncMono non-classical monocytes, mDC myeloid dendritic cells, pDC plasmacytoid dendritic cells, NK natural killer cells, NKT natural killer T cells, MK megakaryocytes.