Mace‐Like Plasmonic Au‐Pd Heterostructures Boost Near‐Infrared Photoimmunotherapy

Author:

Feng Yanlin1ORCID,Ning Xin1,Wang Jianlin1,Wen Zhaoyang1,Cao Fangfang23,You Qing23,Zou Jianhua23,Zhou Xin1,Sun Teng1,Cao Jimin1ORCID,Chen Xiaoyuan2345

Affiliation:

1. Key Laboratory of Cellular Physiology at Shanxi Medical University Ministry of Education and the Department of Physiology Shanxi Medical University Taiyuan 030001 China

2. Departments of Diagnostic Radiology, Surgery, Chemical and Biomolecular Engineering and Biomedical Engineering Yong Loo Lin School of Medicine and Faculty of Engineering National University of Singapore Singapore 119074 Singapore

3. Nanomedicine Translational Research Program NUS Center for Nanomedicine Yong Loo Lin School of Medicine National University of Singapore Singapore 117597 Singapore

4. Clinical Imaging Research Centre Centre for Translational Medicine Yong Loo Lin School of Medicine National University of Singapore Singapore 117599 Singapore

5. Institute of Molecular and Cell Biology Agency for Science, Technology, and Research (A*STAR) 61 Biopolis Drive, Proteos Singapore 138673 Singapore

Abstract

AbstractPhotoimmunotherapy, with spatiotemporal precision and noninvasive property, has provided a novel targeted therapeutic strategy for highly malignant triple‐negative breast cancer (TNBC). However, their therapeutic effect is severely restricted by the insufficient generation of tumor antigens and the weak activation of immune response, which is caused by the limited tissue penetration of light and complex immunosuppressive microenvironment. To improve the outcomes, herein, mace‐like plasmonic AuPd heterostructures (Au Pd HSs) have been fabricated to boost near‐infrared (NIR) photoimmunotherapy. The plasmonic Au Pd HSs exhibit strong photothermal and photodynamic effects under NIR light irradiation, effectively triggering immunogenic cell death (ICD) to activate the immune response. Meanwhile, the spiky surface of Au Pd HSs can also stimulate the maturation of DCs to present these antigens, amplifying the immune response. Ultimately, combining with anti‐programmed death‐ligand 1 (α‐PD‐L1) will further reverse the immunosuppressive microenvironment and enhance the infiltration of cytotoxic T lymphocytes (CTLs), not only eradicating primary TNBC but also completely inhibiting mimetic metastatic TNBC. Overall, the current study opens a new path for the treatment of TNBC through immunotherapy by integrating nanotopology and plasmonic performance.

Funder

National Natural Science Foundation of China

Shanxi Provincial Key Research and Development Project

Publisher

Wiley

Subject

General Physics and Astronomy,General Engineering,Biochemistry, Genetics and Molecular Biology (miscellaneous),General Materials Science,General Chemical Engineering,Medicine (miscellaneous)

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