Fig. 6

Intercellular crosstalk of LEC-CD8⁺ T_CM cells. (a) UMAP diagram annotated by endothelial cell subpopulations. (b) Dot line plot of LEC_CCL21 expression between different groups. (c) Network diagram of inferred ligand‒receptor interactions between the LEC_CCL21 and CD8⁺ T cell subsets. The edge width reflects interaction strength, and the node size is scaled according to cell type abundance. (d) Sankey diagram of chemokine–receptor pairs showing all expressed ligands (left column) and their cognate receptors (right column), with flow widths proportional to the inferred interaction probability. (e) GO enrichment of receptors in the LEC_CCL21-CD8⁺ T_CM interaction. (f) Summary schematic contrasting normal control, PTC and ATC microenvironments. In normal control and PTC microenvironments, LEC-derived CCL21 engages CCR7 on central memory CD8⁺ T cells to promote chemotaxis and tumor surveillance. In ATC, LEC_CCL21 + cell infiltration is reduced, leading to attenuated chemotaxis and accelerated tumor growth in the CD8 + T_CM subset.