Macrophage‐Capturing Self‐Assembly Photosensitizer Nanoparticles Induces Immune Microenvironment Re‐Programming and Golgi‐Responsive Immunogenic Cell Death in Head and Neck Carcinoma

Author:

Zhou Zhi‐hang123,Zhou Xin‐yu34,Zhang Yi‐yi2,Zhao Tong‐Chao1,Li Jiang2,Zhong Lai‐ping1,Pang Yi‐chuan5ORCID

Affiliation:

1. Department of Stomatology Huashan Hospital Fudan University Shanghai 200040 China

2. Department of Oral Pathology Ninth People's Hospital College of Stomatology Shanghai Jiao Tong University School of Medicine Shanghai 200011 P. R. China

3. Department of Oral and Maxillofacial‐Head and Neck Oncology Ninth People's Hospital College of Stomatology Shanghai Jiao Tong University School of Medicine Shanghai 200011 China

4. Shanghai Key Laboratory of Stomatology & Shanghai Research Institute of Stomatology National Clinical Research Center of Stomatology Shanghai 200011 China

5. Department of Nuclear Medicine Shanghai Tenth People's Hospital Tongji University School of Medicine Shanghai 200072 China

Abstract

AbstractHead and neck carcinoma treatment is shifted toward the combination of therapy causing immune checkpoint blockade (ICB) and immunogenic cell death. In this study, a CSFRi‐chimeric TAMCSFR+‐targeting extracellular vesicle (EV@CSFRi) platform is developed and designed an intracellular protoporphyrin conjugated with RVRR peptide sequence for furin‐cleavage to perform Golgi‐targeting and generating ROS (GT‐RG). The graphical abstract illustrates the self‐assembly of GT‐RG nanoparticles into nanofiber through the hydrophily of RVRR and hydrophobicity of RG, and the red line indicates the site of furin cleavage. As is shown in the Graphical abstract, the Golgi‐targeting Protoporphyrin‐RVRR platform is composed with CSFRi‐chimeric extracellular vesicles and forms the tumor‐responsive TAM‐reprogramming bilayers (GT‐RGEV@CSFRi). The GT‐RGEV@CSFRi acted as a multifunctional theranostic platform, which can induce immunogenic cell death and further help modulate TAM, thus suppressing the HNC xenograft model by combination therapy with anti‐PD‐1.

Funder

National Natural Science Foundation of China

China Postdoctoral Science Foundation

Program of Shanghai Academic Research Leader

Publisher

Wiley

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