Self-triggered thermoelectric nanoheterojunction for cancer catalytic and immunotherapy

The exogenous excitation requirement and electron-hole recombination are the key elements limiting the application of catalytic therapies. Here a tumor microenvironment (TME)-specific self-triggered thermoelectric nanoheterojunction (Bi(0.5)Sb(1.5)Te(3)/CaO(2) nanosheets, BST/CaO(2) NSs) with self-built-in electric field facilitated charge separation is fabricated. Upon exposure to TME, the CaO(2) coating undergoes rapid hydrolysis, releasing Ca(2+), H(2)O(2), and heat. The resulting temperature difference on the BST NSs initiates a thermoelectric effect, driving reactive oxygen species production. H(2)O(2) not only serves as a substrate supplement for ROS generation but also dysregulates Ca(2+) channels, preventing Ca(2+) efflux. This further exacerbates calcium overload-mediated therapy. Additionally, Ca(2+) promotes DC maturation and tumor antigen presentation, facilitating immunotherapy. It is worth noting that the CaO(2) NP coating hydrolyzes very slowly in normal cells, releasing Ca(2+) and O(2) without causing any adverse effects. Tumor-specific self-triggered thermoelectric nanoheterojunction combined catalytic therapy, ion interference therapy, and immunotherapy exhibit excellent antitumor performance in female mice.