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向PD-1和TGF-β通路的酶性响应纳米载体可以逆转免疫治疗耐药性,并产生强大的治疗疗效

Ying-Tzu Yen¹, Zhifan Zhang¹, Anni Chen²

¹The Comprehensive Cancer Center of Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing, 210008, China.

Journal of nanobiotechnology

|February 19, 2025

概括

凝酶响应纳米颗粒 (GPNPs) 为肺癌提供双重免疫疗法,增强T细胞和巨细胞的活性. 这种方法有效地抑制瘤生长,并减少副作用,提供了一个有前途的新治疗策略.

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
生物医学工程生物医学工程

背景情况:

免疫检查点抑制剂 (ICI) 已经改变了肺癌治疗,但面临着耐药性和毒性问题.
双重抑制PD-1/PD-L1和TGF-β通路是克服抗性的潜在策略.
现有的组合疗法具有有限的疗效和显著的全身副作用.

研究的目的:

开发和评估新型凝酶反应纳米颗粒 (GPNPs) 用于同时提供抗PD-1 (αPD-1) 和galunisertib (Gal),一种TGF-β受体I抑制剂.
评估GPNPs在抑制肺癌进展方面的疗效和安全性.
阐明GPNP介导的治疗作用对瘤微环境的潜在机制.

主要方法:

构建封装αPD-1和Gal的GPNPs以进行有针对性的传递.
在肺癌模型中进行体内疗效研究,以评估瘤进展的抑制.
使用细胞计测试分析瘤透淋巴细胞 (TIL) 和巨细胞的免疫分析.
转录组分析和组织学评估 (原,αSMA) 来评估细胞外矩阵调制.
宿命映射研究来追踪纤维细胞分化.

主要成果:

GPNPs证明有效抑制肺癌瘤进展,没有可观察到的副作用.
观察到激活和耗尽的TIL和巨细胞在瘤微环境中的显著招募.
转录组数据显示了细胞外基质的调节,由减少原沉积和αSMA表达体现出来.
宿命映射表明纤维细胞过渡到肌纤维细胞的逆转,可能克服"免疫排他性"瘤表型.

结论:

GPNPs代表了双重肺癌免疫治疗的强大平台,结合了αPD-1和Gal的输送.
GPNP策略有效地重塑瘤微环境,并增强抗瘤免疫反应.
这种方法提供了一个有前途的治疗策略,具有改善肺癌治疗和临床翻译的机制性见解.

关键词:

药物耐药性药物耐药性药物耐药性免疫检查点抑制剂免疫检查点抑制剂聚合物纳米颗粒的分子.转化增长因子-β的转化增长因子-β.瘤微环境是一个微环境.

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