Figure 4.
Reciprocal mononuclear phagocyte chemokine signaling shapes the immunosuppressive microenvironment in cHL. (A) Heatmap of reciprocal ligand-receptor interactions between myeloid subsets and T cells implicated in the cHL TME. Point size indicates permutation P value (CellPhoneDB). Color indicates the min-max normalized aggregate mean expression level of ligand and receptor. (B) Model for intercellular interactions between MNP, dysfunctional T cells, and HRSCs in the cHL TME. HRSCs produce CCL22, CCL17, and CCL5 downstream of NF-κB activity, orchestrating T-cell recruitment via indicated ligand-receptor interactions. CCL3, CCL4, and CXCL10 produced by monocytes and macrophages direct positioning of dysfunctional T cells and cDC2s. Widespread inhibitory molecule expression is seen on HRSCs, MNPs, and T cells.

Reciprocal mononuclear phagocyte chemokine signaling shapes the immunosuppressive microenvironment in cHL. (A) Heatmap of reciprocal ligand-receptor interactions between myeloid subsets and T cells implicated in the cHL TME. Point size indicates permutation P value (CellPhoneDB). Color indicates the min-max normalized aggregate mean expression level of ligand and receptor. (B) Model for intercellular interactions between MNP, dysfunctional T cells, and HRSCs in the cHL TME. HRSCs produce CCL22, CCL17, and CCL5 downstream of NF-κB activity, orchestrating T-cell recruitment via indicated ligand-receptor interactions. CCL3, CCL4, and CXCL10 produced by monocytes and macrophages direct positioning of dysfunctional T cells and cDC2s. Widespread inhibitory molecule expression is seen on HRSCs, MNPs, and T cells.

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