摘要：SummarySuccessful immune responses rely on a regulated delivery of the right signals to the right cells at the right time. Here we show that natural killer (NK) and dendritic epidermal γδ T cells (DETCs) use similar mechanisms to spatiotemporally orchestrate conventional type 1 dendritic cell (cDC1) functions in the spleen, skin, and its draining lymph nodes (dLNs). Upon MCMV infection in the spleen, cDC1 clusterize with activated NK cells in marginal zones. This XCR1-dependent repositioning of cDC1 toward NK cells allows contact delivery of IL-12 and IL-15/IL-15Rα by cDC1, which is critical for NK cell responses. NK cells deliver granulocyte-macrophage colony-stimulating factor (GM-CSF) to cDC1, guiding their CCR7-dependent relocalization into the T cell zone. In MCMV-infected skin, XCL1-secreting DETCs promote cDC1 migration from the skin to the dLNs. This XCR1-dependent licensing of cDC1 both in the spleen and skin accelerates antiviral CD8+T cell responses, revealing an additional mechanism through which cDC1 bridge innate and adaptive immunity.Graphical abstractDisplay OmittedHighlights•Upon viral infection in the spleen, NK cells clusterize with cDC1 in the marginal zone•This XCL1/XCR1-dependent interaction allows mutual delivery of activating signals•NK cell GM-CSF directs cDC1 migration to T cell zone boosting CD8+ T cell priming•In the skin, DETCs contact cDC1 via XCL1/XCR1 to promote antiviral CD8+ T cell primingBiological sciences; Immune system; Cell biology
