Type 1 conventional dendritic cells (cDC1s) play a critical role in anti-cancer immunity through priming of naive, tumor-specific CD8⁺T cells in lymph nodes and, importantly, the stimulation and expansion of antigen-experienced CD8⁺ T cells locally within tumor tissue. Recent work suggests that such local orchestration of anticancer T cell immunity in tumors is, at least in part, mediated by a distinct, CCR7-negative (CCR7^neg) MHC-II^high subpopulation of intratumoral cDC1s.

However, how MHC-II^highCCR7^neg cDC1s are retained in the tumour stroma and which mechanisms govern their interactions with tumor-infiltrating T cells remains unclear. Here, we show that MHC-II^highCCR7^neg cDC1s in tumors localize to distinct intratumoral niches populated by NK cells, which is not the case for their CCR7⁺ counterparts. We uncover that NK cells support the function of MHC-II^highCCR7^neg cDC1s through IFNγ production, and that this role is critical to enable cDC1-mediated support of effector responses by tumor-infiltrating CD8⁺ T cells. We identify that IFNγ signalling in MHC-II^highCCR7^neg cDC1s promotes the expression of the carbohydrate-binding protein Galectin-9, which supports the retention of MHC-II^highCCR7^neg cDC1s in tumours and facilitates their stimulatory interactions with tumour-infiltrating CD8⁺ T cells. Together, our data reveal an IFNγ-Galectin-9-dependent pathway by which NK cells sustain the retention and function of intratumoral cDC1s to support effective CD8⁺ T cell responses.