Visible-Light-Triggered Prodrug Nanoparticles Combine Chemotherapy and Photodynamic Therapy to Potentiate Checkpoint Blockade Cancer Immunotherapy.
Jiwoong ChoiMan Kyu ShimSuah YangHee Sook HwangHanhee ChoJeongrae KimWan Su YunYujeong MoonJinseong KimHong Yeol YoonKwangmeyung KimPublished in: ACS nano (2021)
Immune checkpoint blockade is a promising approach for cancer immunotherapy, but many patients do not respond due to the immunosuppressive tumor microenvironment (ITM). Herein, we propose visible-light-triggered prodrug nanoparticles (LT-NPs) for reversing ITM into high immunogenic tumors to potentiate checkpoint blockade immunotherapy. The photosensitizer (verteporfin; VPF), cathepin B-specific cleavable peptide (FRRG), and doxorubicin (DOX) conjugates are self-assembled into LT-NPs without any additional carrier material. The LT-NPs are specifically cleaved to VPF and DOX in cathepsin B-overexpressing cancer cells, thereby inducing cancer-specific cytotoxicity and immunogenic cell death (ICD) upon visible light irradiation. In tumor models, LT-NPs highly accumulate within tumors via the enhanced permeability and retention effect, and photochemotherapy of VPF and DOX induces effective ICD and maturation of dendritic cells to stimulate cross-presentation of cancer-antigens to T cells. Furthermore, LT-NPs with PD-L1 blockade greatly inhibit tumor growth, tumor recurrence, and lung metastasis by initiating a strong antitumor immune response. The photochemotherapy by LT-NPs provides a promising strategy for effective checkpoint blockade immunotherapy.
Keyphrases
- visible light
- photodynamic therapy
- dendritic cells
- immune response
- dna damage
- oxide nanoparticles
- cell death
- papillary thyroid
- cancer therapy
- cell cycle
- end stage renal disease
- ejection fraction
- newly diagnosed
- regulatory t cells
- chronic kidney disease
- endothelial cells
- squamous cell carcinoma
- prognostic factors
- oxidative stress
- lymph node metastasis
- fluorescence imaging
- toll like receptor
- locally advanced
- young adults
- inflammatory response
- cell cycle arrest