CD4+ T cells help license conventional type 1 dendritic cells (cDC1s) to induce CD8+ cytotoxic T lymphocyte (CTL) anticancer responses in human tumors. Activated CD4+ T cells produce IFNβ via the STING pathway, which promotes MHC-I antigen (cross-)presentation by cDC1s and improves their ability to induce CTL anticancer responses. In cooperation with CD40 ligand (L), IFNβ also optimizes the costimulatory and other functions of cDC1s required for CTL response induction. IFN-I-producing CD4+ T cells are present in diverse T-cell-infiltrated cancers and likely deliver "help" signals to CTLs locally, according to their transcriptomic profile and colocalization with "helped/licensed" cDCs and tumor-reactive CD8+ T cells. The presence of IFN-I-producing CD4+ T cells in the TME is associated with overall survival and the response to PD-1 checkpoint blockade in cancer patients. CD4+ T cells provide help to innate immune cells, B cells, and CD8+ T cells. CD4+ T cells help promote the clonal expansion and effector/memory differentiation of CD8+ T cells. CD4+ T-cell help is relayed to CD8+ T cells via DCs via a process called "DC licensing." In mouse studies, CD4+ T cells license DCs via the CD40 ligand (L)-CD40 signaling pathway. The improved costimulatory status of cDC1s contributes to optimal CTL effector and memory differentiation of CD8+ T cells via CD28- and CD27 costimulation. Mouse studies have also shown that IL-12 production is an important feature of licensed DCs. Our transcriptome data from human cDC1s revealed that antigen (cross-)presentation pathways are upregulated by CD4+ T-cell help, and functional studies confirmed that cDC1s but not other human DC subsets can optimally cross-prime CTL responses to cell-associated antigens in response to CD4+ T-cell help. This finding aligns with the idea gleaned from mouse studies that cDC1s have a unique ability to cross-present cell-associated antigens, which is key for CTL-based antitumor immunity. Among the biological processes most strongly upregulated in "helped/licensed" human cDC1s were cytokine-related pathways. CD4+ T cells amplify IL-15R/IL-15 expression in human cDC1s, which promotes the expansion and survival of memory CD8+ T-cell pools. In addition, CD4+ T-cell help results in upregulation of CXCL9/10/11 in "helped/licensed" cDC1s. These chemokines play essential roles in the spatial distribution and function of CXCR3+CD4+ T cells help license conventional type 1 dendritic cells (cDC1s) to induce CD8+ cytotoxic T lymphocyte (CTL) anticancer responses in human tumors. Activated CD4+ T cells produce IFNβ via the STING pathway, which promotes MHC-I antigen (cross-)presentation by cDC1s and improves their ability to induce CTL anticancer responses. In cooperation with CD40 ligand (L), IFNβ also optimizes the costimulatory and other functions of cDC1s required for CTL response induction. IFN-I-producing CD4+ T cells are present in diverse T-cell-infiltrated cancers and likely deliver "help" signals to CTLs locally, according to their transcriptomic profile and colocalization with "helped/licensed" cDCs and tumor-reactive CD8+ T cells. The presence of IFN-I-producing CD4+ T cells in the TME is associated with overall survival and the response to PD-1 checkpoint blockade in cancer patients. CD4+ T cells provide help to innate immune cells, B cells, and CD8+ T cells. CD4+ T cells help promote the clonal expansion and effector/memory differentiation of CD8+ T cells. CD4+ T-cell help is relayed to CD8+ T cells via DCs via a process called "DC licensing." In mouse studies, CD4+ T cells license DCs via the CD40 ligand (L)-CD40 signaling pathway. The improved costimulatory status of cDC1s contributes to optimal CTL effector and memory differentiation of CD8+ T cells via CD28- and CD27 costimulation. Mouse studies have also shown that IL-12 production is an important feature of licensed DCs. Our transcriptome data from human cDC1s revealed that antigen (cross-)presentation pathways are upregulated by CD4+ T-cell help, and functional studies confirmed that cDC1s but not other human DC subsets can optimally cross-prime CTL responses to cell-associated antigens in response to CD4+ T-cell help. This finding aligns with the idea gleaned from mouse studies that cDC1s have a unique ability to cross-present cell-associated antigens, which is key for CTL-based antitumor immunity. Among the biological processes most strongly upregulated in "helped/licensed" human cDC1s were cytokine-related pathways. CD4+ T cells amplify IL-15R/IL-15 expression in human cDC1s, which promotes the expansion and survival of memory CD8+ T-cell pools. In addition, CD4+ T-cell help results in upregulation of CXCL9/10/11 in "helped/licensed" cDC1s. These chemokines play essential roles in the spatial distribution and function of CXCR3+