CCR7+ dendritic cells (activated cDCs) are well known for driving anti-tumor T cell responses. Upon receiving stimulation in the tumor microenvironment (TME), dendritic cells become activated and upregulate CCR7. This drives their migration to tumor-draining lymph nodes, where T cells are primed de novo. However, some activated cDCs remain in the tumor, forming niches with T cells to support their function. It remains unknown what factors drive the formation of these niches. Here, we examine the cell types and the gene expression programs that define activated cDC niches in tumors. We show that CCL19, regulatory T cells (Tregs) and stemlike T cells colocalize with activated cDCs in perivascular niches. Furthermore, we show that both CCL19 and T cells are required for dense activated cDC clusters to form, while Tregs are not required. With spatially resolved transcriptomics, we reveal additional gene programs associated with activated cDC clusters. By perturbing gene expression in T cells, we demonstrate how T cells organize activated cDC niches to support their function. By uncovering the mechanisms that form these niches, this work introduces potential cancer immunotherapies to enhance antitumor T cell responses.