Extended Data Fig. 6: Distinct compositions and functions of myeloid cells in control and CRS patients.
From: Single-cell profiling identifies mechanisms of inflammatory heterogeneity in chronic rhinosinusitis

a, tSNE plots showing expression of marker genes for myeloid subsets defined in Fig. 4a. b, Violin plots of the expression levels of selected genes in mast cell subsets (nonparametric two-sided Wilcoxon rank sum test adjusted by Bonferroni method; full list of P value given in Supplementary Table 3). c, Correlation analysis of the gene expression similarity of DC subsets in CRS and HCC. d, Violin plots of the M1 (top) and M2 (bottom) phenotype score across 10 macrophage clusters with plot center and box corresponding to median and IQR respectively, calculated by the mean expression of corresponding signature genes. e, tSNE plot separately showing the disease-specific distribution of 11 macrophages clusters in four patient groups. The serial number of each cell cluster is the same with Fig. 5a. f, Violin plots of selected gene expression in tissue-resident macrophages with plot center and box corresponding to median and IQR respectively (nonparametric two-sided Wilcoxon rank sum test adjusted by Bonferroni method). g, Violin plots of selected gene expression in all macrophages with plot center and box corresponding to median and IQR respectively (nonparametric two-sided Wilcoxon rank sum test adjusted by Bonferroni method). h, Graphic summary illustrating the cell origins of arachidonic acid metabolic pathway including enzymes, receptors and their alterations in CRS subtypes. EnC, Endothelial cell; EpC, Epithelial cell; Fb, Fibroblast; MC, Mast cell; Mφ, Macrophage; NE, Neutrophil; NK, NK-CX3CR1; PC, Plasma cell; SMC, Smooth Muscle cell. This figure supports Figs. 4, 5.