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Fig. 3 | Genome Medicine

Fig. 3

From: IFN-γ and TNF-α drive a CXCL10+ CCL2+ macrophage phenotype expanded in severe COVID-19 lungs and inflammatory diseases with tissue inflammation

Fig. 3

Human blood-derived macrophages stimulated by eight mixtures of inflammatory factors reveal heterogeneous macrophage phenotypes. a Schematic representation of the single-cell cell hashing experiment on human blood-derived macrophages stimulated by eight mixtures of inflammatory factors from 4 donors. A single-cell antibody-based hashing strategy was used to multiplex samples from different stimulatory conditions in one sequencing run. Here fibro denotes fibroblasts. b The 25,823 stimulated blood-derived macrophages from 4 donors are colored and labeled in UMAP space. c Log-normalized expression of genes that are specific to different conditions are displayed in violin plots. Mean of normalized gene expression is marked by a line and each condition by individual coloring. CPM denotes counts per million. d Stimulation effect estimates of genes that are most responsive to conditions with IFN-γ or TNF-α with fibroblasts comparing to untreated macrophages are obtained using linear modeling. Fold changes with 95% CI are shown. e Fold changes in gene expression after TNF-α and IFN-γ stimulation vs. TNF-α stimulation (left), and TNF-α and IFN-γ vs. IFN-γ stimulation (right) for each gene. Genes in red have fold change > 2, Bonferroni-adjusted P < 10−7, and a ratio of TNF-α and IFN-γ fold change to TNF-α fold change greater than 1 (left) or a ratio of TNF-α and IFN-γ fold change to IFN-γ fold change greater than 1 (right). Genes that are most responsive to either IFN-γ (left) or TNF-α (right) are labeled

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