Fig. 2

Fcmr deficiency alters TMP functional heterogeneity. a t-SNE representation of cell clusters from FACS-sorted tumor mononuclear phagocytes (TMP) isolated from B16 melanoma tumors growing in Fcmr^+/+ and Fcmr^−/−. b t-SNE representation of the FACS-sorted Fcmr^+/+ and Fcmr^−/− TMPs in (a), highlighting the differential clustering of Fcmr^+/+ (gray) and Fcmr^−/− (blue) cells. c t-SNE representation of the cells in (b) with an emphasis on the unassigned Fcmr^−/− cells (red) that were identified by a projection analysis of Fcmr^−/− cells onto Fcmr^+/+ cell clusters. d–f Heat maps identifying signaling pathways that were significantly up- and down-regulated in various cell subsets as determined by gene set variation analysis (GSVA). Plotted values are the z-score normalized GSVA scores, with z-scores computed row wise. Fcmr^+/+ cells were compared to either d cluster 8 from the combined analysis of Fcmr^+/+ and Fcmr^−/− cells; e cluster 1 from the combined analysis of Fcmr^+/+ and Fcmr^−/− cells; or f the unassigned Fcmr^−/− cells from the projection analysis. For (d–f), each row represents a distinct signaling pathway, and each column represents a single cell. The color scale indicates the level of pathway enrichment. The columns are hierarchically clustered using a Pearson correlation-based distance metric and the ward D2 agglomeration method. The rows are sorted in decreasing order of log2 fold changes or linearly-modeled GSVA scores, with the most upregulated pathway appearing at the top and the most downregulated pathway appearing at the bottom. See Supplementary Tables 1 and 2 for examples of differentially regulated pathways. g Ridge plots representing the expression levels of transcription factors that were significantly differentially expressed between unassigned (unsg) Fcmr^−/− TMPs and all Fcmr^+/+ cells