The diagram is divided into several regions: the tumor, tumor margin, and tertiary lymphoid structure (TLS). In the tumor core, CCR7 positive dendritic cells (DCs) with high PD-L1 and low CD40 colocalize with PD-1 high effector CD8 positive T cells. At the tumor margin, CCR7 negative CXCL9 positive conventional type 1 dendritic cells (cDC1s) colocalize with stem-like TCF1 positive CD8 positive T cells. CCR7 high, CD40 positive CD86 positive cDC1s accumulate within stromal immune hubs and contribute to TLS maintenance and support. These cDC1s interact with CD40L positive CXCL13 positive Tfh-like CD4 positive T cells and present antigens to CD8 positive T cells. MregDC interactions in lymphatic-associated regions limit antigen trafficking to tumor-draining lymph nodes (tdLNs). An early tumor microenvironment (TME) recruitment axis shows NK cell-derived chemokines promoting intratumoral cDC1 accumulation, and CXCL9 positive CD206 positive macrophages supporting CXCR3-dependent recruitment of CD8 positive T cells. Arrows indicate proposed directions of interaction, and co-localization denotes spatial association.
Spatiotemporally organized cDC1-centered immune networks and hubs in the TME. Schematic summarizing key cellular circuits and spatial niches in which cDC1s coordinate antitumor immunity. In the tumor core, a tumor-retained CCR7+ DC state (derived from cDC1/cDC2) with reduced costimulatory capacity (PD-L1hi/CD40lo) colocalizes with PD-1hi effector CD8+ T cells. At the tumor margin, CCR7− CXCL9+ cDC1s colocalize with stem-like TCF1+ CD8+ T cells (Piot et al., 2025). CCR7hi, CD40+CD86+ cDC1s accumulate within stromal immune hubs and contribute to TLS maintenance/support, including through CD40-dependent interactions with CD40L+ CXCL13+ Tfh-like CD4+ T cells and ongoing antigen presentation to CD8+ T cells. In parallel, mregDC–Treg interactions in lymphatic-associated regions can limit antigen trafficking to tdLNs and restrain adaptive priming (You et al., 2024). An “early TME recruitment axis” is depicted in which NK cell–derived chemokines (e.g., XCL1/CCL5 and FLT3L) promote intratumoral cDC1 accumulation, while CXCL9+ CD206+ macrophages support CXCR3-dependent recruitment of CD8+ T cells, facilitating the establishment of this cDC1-NK-CD8 circuit. Arrows indicate proposed directions of interaction; “colocalization” denotes spatial association. TME, tumor microenvironment.