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Updated: Sep 9, 2025

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聚合物基的新抗原纳米疫苗与PD-1/PD-L1调节器协同作用,重编程黑色素瘤微环境

Bárbara Carreira¹, Rita C Acúrcio¹, Ana I Matos¹

¹Research Institute for Medicines (iMed.ULisboa), Faculdade de Farmácia, Universidade de Lisboa, Av. Prof. Gama Pinto, 1649-003 Lisbon, Portugal.

Journal of controlled release : official journal of the Controlled Release Society

|August 31, 2025

概括

这项研究开发了一种纳米疫苗,通过增强T细胞激活和克服免疫检查点阻塞来改善癌症免疫疗法. 该纳米疫苗与新型小分子抑制剂结合,有效抑制黑色素瘤瘤的生长并改善T细胞透.

科学领域:

癌症学
免疫学
纳米技术

背景情况:

针对编程细胞死亡蛋白1 (PD-1) 和其连接体PD- L1的免疫检查点阻塞 (ICB) 疗法在癌症治疗中具有前景.
由瘤免疫性差和免疫抑制瘤微环境 (TME) 等因素驱动的对ICB的耐药性限制了治疗效果.
提高瘤免疫性和调节TME的策略对于克服ICB耐药性至关重要.

研究的目的:

开发基于纳米粒子的策略来增强黑色素瘤免疫疗法并克服ICB耐药性.
在黑色素瘤小鼠模型中,评估一个用曼诺斯移植的多乳糖酸 (PLGA) 纳米疫苗,以评估其促进T细胞激活和克服ICB抗性的能力.
将纳米疫苗与单克隆抗体 (αPD- L1) 与新型小分子抑制剂 (SM56) 的疗效进行比较.

主要方法:

开发一种含有黑色素瘤新抗原的PLGA纳米疫苗
将纳米疫苗与αPD- L1或SM56联合给具有攻击性,耐ICB的B16F10黑色素瘤小鼠模型.
评估瘤生长抑制,T细胞透和TME内的免疫抑制细胞群的变化.

主要成果:

纳米疫苗与PD-1/ PD- L1通路调节剂相结合,在B16F10黑色素瘤模型中显著抑制了瘤生长.
在纳米疫苗组合疗法中观察到T细胞透到瘤微环境中的增强.
只有与小分子抑制剂SM56的组合有效降低了TME中的免疫抑制细胞群.

结论:

聚合纳米疫苗有可能克服限制ICB在癌症免疫治疗中的关键抵抗机制.
新型小分子抑制剂,如SM56,为增强黑色素瘤免疫疗法的单克隆抗体提供了有希望的替代品.
纳米疫苗和小分子抑制剂的联合治疗提供了一个可行的策略,以改善ICB耐药黑色素瘤的治疗结果.

关键词:

免疫疗法单克隆抗体纳米疫苗 PD-1/PD-L1 其他小分子 siRNA 其他

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