Anti-PD-L1 biomimetic nanobubbles for ultrasound-triggered reprogramming of cold hepatocellular carcinoma for immunotherapy.
Hepatocellular carcinoma exhibits profound resistance to immune checkpoint blockade due to its dense stromal architecture and immunosuppressive tumor microenvironment with an immune-excluded phenotype
APA
Tu H, Cao Y, et al. (2026). Anti-PD-L1 biomimetic nanobubbles for ultrasound-triggered reprogramming of cold hepatocellular carcinoma for immunotherapy.. Journal of controlled release : official journal of the Controlled Release Society, 392, 114659. https://doi.org/10.1016/j.jconrel.2026.114659
MLA
Tu H, et al.. "Anti-PD-L1 biomimetic nanobubbles for ultrasound-triggered reprogramming of cold hepatocellular carcinoma for immunotherapy.." Journal of controlled release : official journal of the Controlled Release Society, vol. 392, 2026, pp. 114659.
PMID
41592624
Abstract
Hepatocellular carcinoma exhibits profound resistance to immune checkpoint blockade due to its dense stromal architecture and immunosuppressive tumor microenvironment with an immune-excluded phenotype. To overcome this therapeutic challenge, we developed PD-1-displaying biomimetic nanobubbles (NB@CM-H-PD-1) that orchestrate a trimodal strategy combining PD-L1-targeted checkpoint blockade, sonodynamic therapy, and acoustic cavitation-mediated stromal remodeling to transform immunologically "cold" HCC into an immune-responsive state. These engineered nanobubbles comprise a perfluorocarbon core, a lipid-bilayer shell embedded with hematoporphyrin monomethyl ether, and an outer coating of cell membranes derived from PD-1-overexpressing cells. The platform executes a synchronized cascade: membrane-displayed PD-1 mediates tumor-specific targeting while providing checkpoint inhibition; sonosensitizer activation generates reactive oxygen species (ROS) triggering immunogenic cell death; and ultrasound-targeted nanobubble destruction enhances intratumoral penetration through cavitation-induced stromal disruption. In vitro characterization demonstrated that NB@CM-H-PD-1 maintained excellent biocompatibility under physiological conditions while exhibiting potent ultrasound-triggered ROS production and cytotoxic activity. In both subcutaneous and metastatic HCC models, this approach achieved near-complete tumor eradication without systemic toxicity. Comprehensive immunological analyses revealed robust immunogenic cell death induction, dendritic cells (DCs) maturation, enhanced T-cell infiltration with increased IFN-γ secretion, and tumor microenvironment reprogramming that initiated systemic antitumor immunity controlling both primary and metastatic lesions. Thus, our findings establish this biomimetic platform as an effective mechano-chemical-immune synergistic actuator for sensitizing refractory HCC to immunotherapy.
MeSH Terms
Carcinoma, Hepatocellular; Liver Neoplasms; Animals; Immunotherapy; B7-H1 Antigen; Humans; Mice; Cell Line, Tumor; Biomimetic Materials; Programmed Cell Death 1 Receptor; Ultrasonic Therapy; Immune Checkpoint Inhibitors; Tumor Microenvironment; Fluorocarbons; Hematoporphyrins; Mice, Inbred C57BL; Reactive Oxygen Species; Microbubbles
같은 제1저자의 인용 많은 논문 (3)
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