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.