Conventional type 1 dendritic cells (cDC1s) are specialized for cross-presentation of tumor antigens and are critical for the efficacy of immunotherapies, including immune checkpoint blockade (ICB) and adoptive cell therapy. However, their rarity and dysfunction create a major bottleneck to effective CD8 T cell priming. We developed Tim-3-targeted vaccines by conjugating tumor antigens or neoantigens to anti-Tim-3 antibodies and evaluated their activity across multiple tumor models. Tim-3-targeted vaccination delivered antigen to both cDC1s and cDC2s, elicited robust and durable CD8 T cell responses, and enabled cDC2s to cross-present antigen with efficiency comparable to cDC1s. In CD11c-beta-catenin inactive mice, which model beta-catenin-driven DC dysfunction, Tim-3-targeted vaccination restored cross-priming and counteracted DC-mediated immunosuppression. In Batf3-/- mice lacking cDC1s, Tim-3-targeted vaccines still induced substantial CD8 T cell priming and anti-tumor efficacy, although at lower levels than in wild-type mice, demonstrating that cDC1s contribute to but are not essential for vaccine activity. Tim-3-targeted vaccination also outperformed benchmark cDC1-targeted vaccination in the gp100 model. Importantly, an anti-Tim-3-based vaccine targeting the LLC neoantigen mRiok1 elicited strong anti-tumor activity in both wild-type and Batf3-/- mice, in contrast to prior reports that mRiok1 peptide vaccination failed even when combined with anti-CTLA-4 or anti-PD-1 ICB. Strikingly, a single dose of anti-Tim-3-Adpgk eradicated large established MC38 tumors in a CD8 T cell-dependent manner. Together, these findings establish Tim-3-targeted vaccination as a next-generation cancer vaccine platform that broadens APC engagement, reduces reliance on cDC1s, and overcomes DC-imposed barriers to anti-tumor immunity.