Fig 2: Residual cDCs in patients with ALL lose their specialization into distinct functional lineages(A and B) Flow cytometry analysis depicting the frequencies of (A) cDC1 (CD141HighCD1c−), cDC2-3 (CD141Low/−CD1c+), and cDC4-5 (CD141Low/−CD1c−) and of (B) CD141HighCLEC9A+, CD141Low/−CLEC9A+, and CD141Low/−CLEC9A− cDCs in the PBMCs of healthy donors (n = 18) and patients with ALL (n = 8 B-ALL, n = 5 T-ALL). Median ± interquartile range; p values: Mann-Whitney U test.(C) Workflow to conduct single-cell RNA sequencing (scRNA-seq) of the non-malignant PBMC fraction of healthy donors (n = 6) and patients with ALL (n = 4 B-ALL, n = 2 T-ALL) (GEO: GSE304657).(D and E) UMAP dimensional reduction of 12792 PBMC DCs from six healthy donors and 24,138 PBMC DCs from six patients with ALL showing DC subsets and gene expression of major DC markers by scRNA-seq (GEO: GSE304657).(F) DGE heatmap depicting average relative expression of the top 10 genes found in each healthy (n = 6) DC subset and showing dysregulation of the same genes within each respective ALL (n = 6) DC subset (GEO: GSE304657).