Researchers reported a contact-dependent “cross-dressing” mechanism explaining how dendritic cells amplify tebentafusp-mediated T-cell activity against tumor cells. The work shows dendritic cells can boost tebentafusp-driven T-cell activation, cytokine release and cytotoxicity, adding a mechanistic layer to the drug’s immunology. For developers, the findings point to how antigen-presenting cells may shape response intensity and could inform combination strategies or biomarkers tied to dendritic cell states. —