Fig. 3: Tumour-residing CCR7⁺ DCs undertake an “exhausted” state with duration in the tumour, attenuated by anti-PD-L1 treatment.

a Expression of MHC-II transcripts and Cd74 over pseudotime in tumour DCs. Local regression (loess) was fit to scaled expression values. b Gene signature scores for “GO:BP dendritic cell antigen processing and presentation (GO:0002468)” by CCR7⁺ DC cluster. c Scaled enrichment scores of scRNA-seq of all DCs for “GO:BP DC antigen processing and presentation” and CCR7⁺ DC signature genes, coloured by pseudotime. d GSEA of Ccr7_DC.3 versus Ccr7_DC.1. Only significant pathways (Benjamini-Hochberg-adjusted p values (P-adj) < 0.05) are shown. e Differential gene expression between Ccr7_DC.1 and Ccr7_DC.3. Significant differentially expressed genes (DEG, P-adj < 0.01) from “Hallmark inflammatory response” are highlighted in red. f Milo differential abundance analysis. Bee-swarm plot shows treatment-associated differences in overlapping cellular neighbourhoods (individual points). Differentially abundant neighbourhoods at FDR < 0.05 are coloured. ‘Mixed’ refers to neighbourhoods where cells do not predominantly (>70%) belong to a single cluster. g Differential gene expression between Ccr7_DC.2 and Ccr7_DC.3. DEGs (P-adj < 0.01, log₂Fold-change > 0.5) are coloured. h Flow cytometry of OX40L expression (OX40L^+/Hu-CD4 reporter mice) on CCR7⁺ DC from MC38-Ova tumours and their dLN. Two-sided Wilcoxon rank-sum test (b), two-sided Wald test with Benjamini-Hochberg multiple testing correction (e, g), or paired two-sided student’s t-test (h) were used. Data are shown as box (median; box, 25^th and 75^th percentile; whiskers, 1.5*inter-quartile range) and violin plots (b), or means ± s.d. (h). Points represent independent mice (h). The results shown in h are from one experiment (n = 5 animals), representative of two independent experiments.