An Ion‐Enhanced Oncolytic Virus‐Like Nanoparticle for Tumor Immunotherapy. Issue 45 (12th October 2022)

• Record Type: Journal Article
• Authors: Wu, Fan; Li, Yanli; Meng, Yun; Cai, Xuechao; Shi, Jieyun; Li, Jinjin; Chen, Yang; Zhang, Li; Meng, Xianfu; Li, Huiyan; Jiang, Xingwu; Fu, Zhenxiao; Wu, Yelin; Bu, Wenbo
• Is Part Of: Angewandte Chemie international edition. Volume 61:Issue 45(2022)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2022-10-12
• Subjects: Ion -- Oncolytic Virus-Like -- T Cell Activation -- T Cell Recruitment -- Tumor Immunotherapy; Chemistry -- Periodicals; 540
• DOI: 10.1002/anie.202210487
• Languages: English
• ISSNs: 1433-7851

Abstract

Abstract: T lymphocytes (T cells) are essential for tumor immunotherapy. However, the insufficient number of activated T cells greatly limits the efficacy of tumor immunotherapy. Herein, we proposed an oncolytic virus‐mimicking strategy to enhance T cell recruitment and activation for tumor treatment. We constructed an oncolytic virus‐like nanoplatform (PolyIC@ZIF‐8) that was degraded in the acidic tumor environment to release PolyIC and Zn 2+ . The released PolyIC exhibited an oncolytic virus‐like function that induced tumor cell apoptosis and promoted T cell recruitment and activation through a tumor antigen‐dependent manner. More importantly, the released Zn 2+ not only enhanced T cell recruitment by inducing CXCL9/10/11 expression but also promoted T cell activation to increase interferon‐γ (INF‐γ) expression by inducing the phosphorylation of ZAP‐70 via a tumor antigen‐independent manner. This Zn 2+ ‐enhanced oncolytic virus‐mimicking strategy provides a new approach for tumor immunotherapy. Abstract : An oncolytic virus‐mimicking strategy is proposed to enhance T cell‐mediated tumor immunotherapy by synthesizing an ion‐enhanced nanoplatform PolyIC@ZIF‐8. This nanoplatform not only mimics an oncolytic virus‐like function by inducing cell apoptosis to recruit T cells in a tumor antigen‐dependent manner but also releases Zn 2+ to enhance T cell recruitment and activation in a tumor antigen‐independent manner.