期刊
BIOMATERIALS
卷 283, 期 -, 页码 -出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.biomaterials.2022.121466
关键词
Chemiluminescence resonance energy transfer; Sonodynamic therapy; Cancer immunotherapy; Carbon dioxide; Reactive oxygen species
资金
- Basic Science Research Program, National Research Foundation of Korea (NRF) [2018R1A2B3006080, 2020R1A6A3A13065439]
- Korea Basic Science Institute (National research Facilities and Equipment Center)
- [2020R1A6C101A191]
- National Research Foundation of Korea [2020R1A6A3A13065439] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Sonodynamic therapy (SDT) has emerged as a promising alternative to photodynamic therapy for treating deeply located tumors accessible by ultrasound. However, the therapeutic potential of conventional sonosensitizers is limited. This study reports immunostimulatory nanoparticles (iCRET NPs) for sonoimmunotherapy, which amplify the reactive oxygen species (ROS) production and induce immunogenic cell death in the tumor microenvironment (TME). The iCRET NPs effectively inhibit tumor growth and metastasis when combined with anti-PD-1 antibodies.
Sonodynamic therapy (SDT) has recently emerged as a promising alternative to photodynamic therapy because of its applicability in treating deeply located tumors accessible by ultrasound (US). However, the therapeutic potential of conventional sonosensitizers is limited by the low quantum yield of reactive oxygen species (ROS) and poor immune responses eliciting canonical apoptosis of cancer cells. Herein, we report chemiluminescence resonance energy transfer (CRET)-based immunostimulatory nanoparticles (iCRET NPs) for sonoimmunotherapy, which not only amplify the ROS quantum yield of sonosensitizers but also generate carbon dioxide (CO2) bubbles to induce immunogenic cell death in the tumor microenvironment (TME). Owing to their CRET phenomena responsive to H2O2 in the TME, iCRET NPs exhibit strong cytotoxicity to cancer cells by producing a large quantity of ROS. Additionally, iCRET NPs effectively induce CO2-mediated immunogenic cell death by rupturing the cancer cell membrane in the presence of US, leading to the release of bare damage-associated molecular patterns, such as HSP 70 and HMGB1. Consequently, when iCRET NPs are combined with anti-PD-1 antibodies, iCRET NPs exhibit synergistic effects in 4T1 tumor-bearing mice, in which antitumor immunity is remarkably amplified to inhibit tumor growth and metastasis.
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