Fig. 1

Schematic illustration of PDT, PTT, and PIT including Jablonski diagram, Type-I and Type-II mechanism of PDT, and ICD and reversal of TME in PIT. The interaction between incident photons and chromophores leads to an electron in the ground state (S0) being excited to a transient high-energy singlet state (S1). Subsequently, the electron in the excited S1 state undergoes intersystem crossing (ISC), forming a more stable and longer-lived triplet state (T1). This T1 state interacts with various substances through Type I and Type-II pathways, generating reactive oxygen species (ROS), which is the principle of PDT. Internal conversion (IC), the primary mechanism of PTT, involves the electron in the S1 state relaxing non-radiatively back to S0, releasing part of its energy as heat, causing a sharp increase in local tumor temperature. Both PDT and PTT can initiate an antitumor immune response via the mechanism of ICD. This process involves the release of a series of danger-associated molecular patterns (DAMPs) and cytokines, promoting the recruitment and maturation of APCs, cross-presentation, and phagocytosis. The tumor antigens are then presented to T cells, ultimately activating the antitumor immune response. This is the main mechanism of PIT. PTT photothermal therapy. PDT photodynamic therapy. PIT photoimmunotherapy. ICD immunogenic cell death. iDC immature dendritic cell. mDC mature dendritic cell. M1 type 1 macrophages. M2 type 2 macrophages. NKT2 naturalkiller T. MDSC myeloid-derived suppressor cells. NK1 natural killer 1. The figure was created with BioRender.com