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

Intratumoral cDC1–T cell clustering in TC-In/DC-In tumors is linked to the highest likelihood of tumor rejection, unlike TC-In/DC-Ex tumors that persist despite T-cell infiltration.

• Why it matters: Antitumor T-cell killing depends on cDC1 interactions, but how these contacts inside tumors shape immune organization and tumor fate is not well defined.
• What they did: Using a tumor array model, the study defined three spatial immunotypes (TC-In/DC-In, TC-In/DC-Ex, TC-Ex/DC-Ex) and assessed cDC1–T cell proximity, costimulatory molecule expression, and effector T-cell persistence.
• The result: In TC-In/DC-In tumors, cDC1s directly interact with T cells, upregulate costimulatory molecules, and sustain effector responses; chemokine modulation via CXCL9, CCL5, and XCL1 reshapes infiltration to promote intratumoral cDC1–T cell clusters and improve rejection.

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