Fig. 1.

Schematic illustration of NP/mDs interacting with primary tumors and immunocytes to remodel the local TME. The rapid burst of redox-responsive NPs inside tumor cells endowed dying cells with immunogenicity, which primed T cell response indirectly via bystander DCs. The camouflaged mDs transferred the trapped allogeneic TA to imDC surface for biometric recognition, a process termed cross-dressing. The last mechanism involved the presentation of allogeneic TA-MHC and costimulatory molecules on the surface of bioengineered NP/mDs, which gave them the potential to directly initiate immune response. Finally, the upregulated IL-12 and IFN-γ continued to break tolerance and license T cells to augment antitumor immunity. The blockade of PD-1/PD-L1 coupling unleashed host immunosuppression, resulting in the local regression of primary tumors and distant anti-metastasis of traveled tumors.