肿瘤微环境
细胞毒性T细胞
免疫系统
细胞毒性
肿瘤缺氧
癌症研究
先天免疫系统
生物
自然杀伤细胞
细胞生物学
抗原
化学
效应器
细胞
免疫学
淋巴细胞
巨噬细胞
淋巴因子激活杀伤细胞
免疫疗法
细胞内
癌细胞
癌症免疫疗法
免疫
肿瘤进展
癌症
作者
Jingqiao Wang,Lingyang Meng,Fanling Meng,Zhang Tingjie,Guofeng Cheng,Xiguang Chen,Ya Liu
出处
期刊:Small
[Wiley]
日期:2025-09-18
卷期号:21 (44): e05680-e05680
标识
DOI:10.1002/smll.202505680
摘要
Natural killer (NK) cells, as critical effectors of the innate immune system, can directly recognize and kill tumor cells without prior antigen priming. However, NK cell activity is hindered by hypoxia and immunosuppressive factors in the tumor microenvironment. Herein, NK cell membrane (NKCM)-camouflaged hypoxia-responsive nanoparticles (HSF@NK) are developed to co-deliver ferrocene (Fc) and carbonic anhydrase IX (CAIX) siRNA for an NK cell-mimicking anticancer strategy, enhancing tumor-specific cytotoxicity and reversing the immunosuppressive tumor microenvironment. HSF@NK achieves tumor targeting and immune evasion by retaining NKCM proteins. Hypoxic tumor microenvironment triggers the release of Fc and CAIX siRNA, decreasing the intracellular pH by downregulating CAIX to accelerate Fc-involved Fenton reaction, and amplifies oxidative damage in tumor cells, while remaining non-cytotoxic to normal cells in vitro. The resulting oxidative stress elicited immunogenic cell death, dendritic cells maturation, and cytotoxic T lymphocyte infiltration, while NKCM proteins promoted M1 macrophage polarization. HSF@NK significantly inhibited tumor growth (≈85.0%) in B16F10 murine tumor models. When combined with anti-PD-L1, HSF@NK further enhanced tumor suppression (≈92.4%) and established long-term immunity in 4T1 tumor models. This approach offers a paradigm shift in the design of NK cell-inspired nanomedicines and paves the way for reliable strategies for solid tumor therapy.
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