Intratumoral cDC1–T cell clusters serve as sites of local costimulation to enhance CTL-mediated tumor rejection

T cells are essential for antitumor immunity, but their ability to eliminate tumors depends on interactions with type 1 conventional dendritic cells (cDC1s). cDC1s are known for cross-presenting tumor-derived antigens in lymph nodes to prime T cells, but their role within tumors remains less well understood. Here, we use a tumor array model to investigate how cDC1–T cell interactions influence immune responses and tumor fate. We show that the spatial distribution of both cDC1s and T cells determines whether a tumor can be rejected. We defined three immunotypes based on the spatial distribution of T cells and cDC1s: T cell–inflamed/dendritic cell-inflamed (TC-In/DC-In) tumors, where T cells and cDC1s coinfiltrate the tumor; T cell–inflamed/dendritic cell-excluded (TC-In/DC-Ex) tumors, where T cells infiltrate but cDC1s remain at the periphery; and T cell–excluded/dendritic cell-excluded (TC-Ex/DC-Ex) tumors, which lack both cDC1 and T cell infiltration. TC-In/DC-In tumors are most likely to undergo rejection, whereas TC-In/DC-Ex tumors persist despite T cell infiltration. Within TC-In/DC-In tumors, cDC1s interact directly with T cells, upregulate costimulatory molecules, and sustain effector T cell responses, while cDC1s in TC-In/DC-Ex tumors express higher migration-associated genes, suggesting they may exit the tumor. We further show that chemokine modulation, particularly through CXCL9, CCL5, and XCL1, can reshape immune infiltration patterns to promote intratumoral cDC1–T cell clustering and improve tumor rejection. These findings reveal an important role of cDC1 in sustaining effective antitumor immunity and highlight spatially organized cDC1–T cell clusters as critical hubs for local T cell activation.