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通过重新编程免疫抑制瘤微环境以减轻缺氧缓解来增强光动力免疫疗法

Mengying He¹, Mengyao Zhang¹, Tao Xu²

¹Jiangsu Key Laboratory of Neuropsychiatric Diseases, College of Pharmaceutical Sciences, Soochow University, Suzhou 215123, China.

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

|February 23, 2024

概括

这项研究开发了一个纳米平台来克服瘤缺氧,增强光动力免疫疗法. 治疗促进了癌细胞死亡和免疫反应,导致瘤根除和预防复发.

科学领域:

生物医学工程生物医学工程
癌症研究癌症研究
免疫治疗是一种免疫疗法.

背景情况:

瘤低氧阻碍光动力学疗法 (PDT) 和免疫疗法,通过减少活性氧物种和促进免疫抑制瘤微环境 (TME).
缺氧会影响免疫抑制性瘤相关巨细胞 (TAMs) 和编程死亡配体1 (PD-L1) 的表达,进一步阻碍抗瘤免疫力.
现有的治疗方法在克服缺氧诱导的免疫抑制以有效治疗癌症方面面临挑战.

研究的目的:

设计一个纳米平台,同时缓解缺氧和免疫调节,以增强光动力免疫疗法.
为了研究光动力疗法,化疗和免疫检查点阻塞在低氧瘤模型中的综合效应.
开发一种用于治疗缺氧和免疫抑制癌症,特别是乳腺癌的新策略.

主要方法:

一个含有二氧化 (MnO2) 的阿尔伯明纳米平台被设计为同时提供IR780 (光敏化剂),NLG919 (诱导免疫检查点阻塞) 和一个帕克利塔塞尔 (PTX) 二次体.
该纳米平台利用MnO2产生氧气,以提高PDT和化疗的疗效,促进免疫细胞死亡 (ICD).
该研究评估了纳米平台通过减少M2-TAM透和PD-L1表达来重塑TME的能力,从而增强细胞毒性T淋巴细胞 (CTL) 活性.

主要成果:

基于MNO2的纳米平台成功产生了氧气,促进了PDT和PTX化疗,导致ICD增加和瘤特异性CTLs的扩张.
低氧缓解和免疫检查点阻塞调节了TME,降低了M2-TAMs和PD-L1表达,从而增强了CTL透和有效性.
综合治疗策略导致显著的原发性瘤根除和几乎完全预防瘤复发和转移.

结论:

开发的纳米平台有效地解决瘤缺氧和免疫抑制问题,显著提高光动力学免疫治疗结果.
这种方法表明,通过将ICD诱导与TME调制相结合,改善乳腺癌治疗的有希望的策略.
该研究为通过综合治疗策略治疗各种缺氧和免疫抑制性癌症提供了一个多功能平台.

关键词:

减轻低氧的缓解作用免疫检查站封锁免疫检查站封锁免疫抑制的瘤微环境光动力免疫疗法光动力免疫疗法与瘤相关的巨细胞.

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