Lymphatic transport is a key mechanism for maintaining tissue-specific adaptive immune responses, but exacerbated lymphatic growth can shape immune-suppressive environments and promote metastasis in solid tumors. We recently demonstrated that intratumoral expansion of melanoma-associated lymphatic vasculature is driven highly invasive lymphatic states characterized by high expression of Notch receptors and ligands. These tip-like lymphatic endothelial cells depended upon oxidative phosphorylation (OXPHOS) for their expansion and directly facilitated tumor but inhibited dendritic cell (DC) migration to the draining lymph node (dLN). Consequently, lymphatic-specific knockout of OXPHOS was sufficient to restrain intratumoral lymphatic expansion, prevent metastasis, and promote response to immunotherapy. How residual, mature lymphatic vessels mechanistically shape DC function and thereby anti-tumor immune surveillance, remains unclear. Here we test the hypothesis that intratumoral lymphatic vasculature disrupts DC migration kinetics leading to fewer mature DCs in the dLN and dysfunctional T-cell priming. Using a lymphatic-specific model of impaired OXPHOS (Prox1:Cre^ERT2;Uqcrq^fl/fl; Uqcrq^iProx), which efficiently prevents intratumoral lymphangiogenesis but leaves pre-existing, mature vessels intact, we find no significant difference in DC abundance in B16F10.OVA.VEGFC tumors and dLNs. Consistent with the literature, phenotypic analysis revealed that despite high co-expression of CD80/86 on DCs in the tumor, migratory DCs (migDC, MHCII^hiCD11c^int) in the dLNs of control mice largely lacked these costimulatory molecules, suggesting reduced maturation. This phenotype was rescued in Uqcrq^iProx mice, where dLN migDCs exhibited a significantly more mature phenotype, with CD80/86 co-expression commensurate with migDCs in the primary tumor. Furthermore, we found that tumor-specific CD8⁺ T cells (OT-1 TCR-tg) in the dLNs of Uqcrq^iProx1 mice exhibited more effector-like phenotypes and less progenitor or terminally exhausted states. These findings are consistent with the hypothesis that lymphatic normalization optimizes tumor immune surveillance and ongoing work will investigate the specific mechanisms underlying lymphatic-dependent changes in migDC dynamics.