Dendritic cells as central coordinators of oncolytic virus-induced antitumor immunity.

Antigen-presenting cells shape the efficacy of cancer immunotherapies by providing essential signals required for antitumor T-cell response. Dendritic cells (DCs) are central to oncolytic virus (OV)-induced antitumor immunity because they couple tumor-antigen acquisition to cross-presentation and T-cell priming in tumor-draining lymph nodes. In tumors, however, DC recruitment, maturation, migration, and antigen-processing functions are frequently impaired by immunosuppressive and metabolic constraints. OVs can partially reprogram this axis by selectively infecting and lysing tumor cells, increasing tumor-antigen availability, and providing pathogen and damage-associated cues that facilitate DC activation. When these events are appropriately coordinated, OV therapy can enhance DC-mediated cross-presentation, promote priming of tumor-reactive CD8⁺ T-cells, support memory formation, and facilitate antigen spreading. At the same time, excessive antiviral load, unfavourable dosing or route, and tolerogenic or metabolically impaired DC states can limit these benefits. In this review, we discuss how OV platforms engage distinct DC subsets, how route, schedule, and engineering strategies shape DC-dependent priming in tumors and draining lymph nodes, where direct mechanistic evidence remains incomplete. We also highlight translational opportunities to monitor and therapeutically augment DC responses in OV-based cancer immunotherapy.