Immune regulation of DC subsets in tumor microenvironment (TME). (A) cDCs uptake tumor-derived antigens and migrate into drai-ning LNs in order to present antigens to T cells. cDC1s are requi-red for both CD4+ and CD8+ T-cell priming, but cDC2s are needed only for CD4+ T cells. The migration of cDCs between LNs and TME is driven by CCR7-CCL21 chemotaxis. The recruitment of activated T cells into TME is dependent on CXCL9 and CXCL10, ligands of CXCR3, produced by cDC1s. The co-stimulatory molecules expressed by DCs positively or negatively regulate T-cell activation. NK cells induce the recruitment of cDC1s via CCL5 and XCL1 chemokine secretions, and cDC1s increase NK-cell activation via IL-12 production. Upon tumor antigen uptake, cDCs are genetically programmed to convert into regulatory DCs expressing PD-L1. (B) CCL2 expressed in TME recruit blood-circulating monocytes, which can differentiate into moDCs. Whereas moDCs can become CD103+ DCs activating CD8+ T cells, they can also be regulatory DCs, with the expression of PD-L1 and CD209, producing IL-10. (C) pDCs produce considerable type I IFNs activating cDCs. However, immunosuppressive cytokines (IL-10 and TGF-β1) produced by tumor cells induce the con-version of pDCs into ICOS-L-expressing tolerogenic pDCs, which promote ICOS-positive regulatory CD4+ T cells to produce IL-10.