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纯能受体纳米免疫增强剂在肝细胞癌中增强化学免疫疗法的有效性

Jialiang Zhang^1,2, Jinyu Zhang^1,2,3, Qiang Feng^1,2

¹Innovation Center for Cancer Research, Clinical Oncology School of Fujian Medical University, Fujian Cancer Hospital, Fuzhou 350014, PR China.

Biomaterials research

|November 10, 2025

概括

这项研究引入了ivermectin-MnO2纳米复合物 (IMN) 来促进肝癌的化疗免疫疗法. IMN增强免疫细胞对瘤的激活,通过放大细胞外ATP/P2X7R/NLRP3炎症酶通路来提高治疗效率.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
纳米技术纳米技术

背景情况:

肝细胞癌 (HCC) 的化疗免疫治疗受到化疗诱导细胞死亡免疫性差的限制.
细胞外腺三酸盐 (eATP) /P2X7纯能受体 (P2X7R) /NLRP3炎症酶通路在树突细胞 (DCs) 中的不足激活有助于这种限制.

研究的目的:

开发P2X7R向的纳米免疫增强剂,以增强HC的化疗诱导免疫细胞死亡 (ICD) 的免疫性.
研究ivermectin-MnO2纳米复合物 (IMN) 在克服化疗免疫疗法耐药性的潜力.

主要方法:

设计ivermectin-MnO2纳米复合体 (IMN) 的目标是P2X7R.
评估IMNs对脂质体多克索鲁比 (LD) 诱导的ICD和P2X7R敏感性的影响.
评估MnO2成分在缓解瘤缺氧和防止eATP降解方面的作用.
在DC中对eATP/P2X7R/NLRP3炎症酶组级联激活的分析.
在HCC小鼠模型中测试IMN疗效与抗PD-L1抗体和LD结合.

主要成果:

IMNs增强了LD诱导的ICD,并增加了P2X7R对eATP的敏感性.
IMN中的MnO2成分降低了瘤缺氧和CD39/CD73表达,防止了eATP降解.
IMNs强烈地激活了DCs中的eATP/P2X7R/NLRP3炎症酶级联,产生了强大的抗瘤免疫反应.
与IMN,抗PD-L1和LD的联合治疗显著抑制了各种HCC小鼠模型中的瘤生长.

结论:

在ICD期间,IMN有效地放大了DC中的NLRP3炎症酶级联.
IMNs代表了一种有前途的策略,以提高HCC化疗免疫疗法的疗效.
通过IMN针对eATP/P2X7R/NLRP3通路,为癌症治疗提供了一种新的方法.

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