Extended Data Fig. 7: CD4 ACT therapy predominantly recruits immature monocytes into the tumour microenvironment and drives the acquisition of IFN-activated effector phenotypes.
From: CD4+ T cell-induced inflammatory cell death controls immune-evasive tumours
a, Differentially expressed genes comparing samples from CD4 ACT-treated versus non-treated (NT) mice. Genes with –log Q-values >200 are shown in orange. b, Gene set enrichment analysis for the “GOBP_RESPONSE_TO_TYPE_I_INTERFERON” (top) and “GOBP_INTERFERON-GAMMA_MEDIATED_SIGNALING_PATHWAY” (bottom) gene sets. c, UMAP plots with Leiden clusters for monocytes and macrophages of CD4 ACT treated tumours. d, Corresponding expression levels and expression cell fractions of selected signature genes for the individual Leiden clusters and (e) pseudotime inference using slingshot. f, Heatmap of differentially expressed genes along the pseudotime trajectory of the indicated Leiden clusters representing the monocyte-macrophage (mono-mac) effector differentiation path. g, Experimental protocol (left), and t-SNE heatmaps of multiparametric flow cytometry for HCml12 melanoma single cell suspensions showing the indicated markers (right). h, Left: Corresponding annotation of immune of immature monocytes (CD11b+ Ly6Chi), mature monocytes (CD11b+ Ly6clo), mature macrophages (CD11b+ F4/80+ iNOS-), iNOS+ mono-macs (CD11b+ Ly6Chi iNOS+), dendritic cells (CD11b+ MHC-II+ CD11c+ F4/80-), endogenous lymphocytes (CD11b- CD11c-), and neutrophils (CD11b+ Ly6G+). Right: Annotated t-SNE plots quantifying the immune cell composition of HCmel12 melanomas at the indicated time points.
