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克服EGFR介导的树突细胞功能障碍以提高EGFR突变NSCLC的抗瘤免疫力,通过精确地针对CD73与pH响应的纳米载体

Xiaoling Shang¹, Xudong Geng², Zixu Wang¹

¹Department of Medical Oncology, Qilu Hospital of Shandong University, 107 Wenhuaxi Road, Jinan, Shandong, 250012, China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|October 27, 2025

概括

非小细胞肺癌中的EGFR突变通过损害树突细胞来阻碍抗瘤免疫力. 一种针对CD73-adenosine通路的新型纳米药物克服了这一问题,提高了免疫治疗的有效性.

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:

非小细胞肺癌 (NSCLC) 的EGFR突变与免疫检查点抑制剂的不良反应有关.
瘤微环境 (TME) 通过EGFR突变的调节会损害抗瘤免疫力,特别是树突细胞 (DC) 功能.

研究的目的:

阐明EGFR突变诱导NSCLC中免疫抑制性TME的机制.
开发一种新的纳米药物,以克服EGFR突变介导的免疫疗法耐药性.

主要方法:

用临床样本分析,多组学和体内小鼠模型来研究EGFR突变对TME的影响.
开发和应用一种对pH响应的纳米药物 (^F127ZIF-8_AB680) 针对CD73-adenosine通路.
在EGFR突变NSCLC模型中与PD-1阻断相结合的纳米药物疗效的评估.

主要成果:

发现EGFR突变会通过ERK/c-Jun轴增加腺素的产生来损害DC成熟和CD8⁺ T细胞的原始化.
纳米药物F127ZIF-8AB680有效地向了酸性TME中的CD73-腺素通路.
与纳米药物和PD-1阻断的联合治疗显著抑制了瘤生长,并在EGFR突变NSCLC小鼠模型中改善了生存率.

结论:

由于EGFR突变通过腺生产破坏DC功能,从而产生免疫抑制的TME.
对pH敏感的纳米药物^F127ZIF-8_AB680显示出通过调节TME,有望克服EGFR突变NSCLC中的免疫疗法耐药性.

关键词:

发生EGFR突变的原因 F127ZIF-8AB68080 F127ZIF-8AB680 F127ZIF-8AB680 F127ZIF-8AB680 F127ZIF-8AB680 F127ZIF-8AB680 氨酸 (Adenosine) 是一种氨酸.树突细胞是一种树突细胞.免疫检查点抑制剂免疫检查点抑制剂非小细胞肺癌的肺癌.

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