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基性瘤细胞衍生的细胞外囊泡刺激CD8T细胞响应在结直肠癌

Travis J Gates¹, Dechen Wangmo¹, Xianda Zhao²

¹Department of Pharmacology, University of Minnesota Medical School, Minneapolis, MN, USA.

Molecular therapy oncolytics

|October 12, 2023

概括

在结直肠癌模型中,缺乏miR-424的改性全基性瘤衍生的细胞外囊 (TEV) 可以促进CD8+T细胞的反应,并抑制瘤生长. 这种方法显示出克服免疫检查点抑制剂耐药性的前景.

科学领域:

免疫学免疫学免疫学
在瘤学瘤学.
生物技术是生物技术.

背景情况:

大多数结直肠癌 (CRC) 患者表现出微卫星稳定性,导致对免疫检查点抑制剂 (ICI) 的耐药性.
瘤衍生的细胞外囊泡 (TEVs) 与ICI耐药性有关.
以前的研究表明,没有miR-424的自身TEV可以在CRC模型中诱导抗瘤免疫反应.

研究的目的:

调查所有原型TEVs是否被修改为缺乏miR-424,可以诱导CD8+T细胞反应并抑制瘤生长.
探索TEV介导免疫反应的机制,重点关注树突细胞 (DC) 相互作用.
在临床前癌症模型中评估改性全基 TEV 的安全性和有效性.

主要方法:

在CT26瘤模型中预防使用缺乏miR-424的MC38TEV.
评估CD8+T细胞透到瘤中的情况.
在体外研究TEVs的DC内部化.
对DC介导的抗瘤效应的评估,暴露于修改后的TEVs.
对周围血液中细胞因子水平的分析.

主要成果:

在没有miR-424的MC38TEVs的预防性施用显著增加了CT26瘤内的CD8+T细胞.
这种异性TEV效应特异于CT26瘤,并未在B16-F10黑色素瘤中观察到.
状细胞被证明可以内化TEVs,这表明免疫激活的机制.
与暴露于野生型TEVs的DC相比,预暴露于改性TEVs的自身DC显示出增强的瘤生长抑制和增加的CD8+T细胞水平.
修改后的TEV被很好地容忍,而外周血液中细胞因子水平没有增加.

结论:

没有免疫抑制因子的修饰异质TEVs可以引起强大的CD8+T细胞反应.
这些修改后的TEV显示出限制瘤生长的潜力,为CRC的ICI耐药性提供了一种新的策略.
这些发现支持开发基于TEV的免疫疗法,用于微卫星稳定的结直肠癌.

关键词:

在T细胞,T细胞.一个全物质的全物质性.结肠直肠癌是什么意思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瘤的细胞外囊泡.

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