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单链IL-23由CAR T细胞分泌改善了瘤控制和对固体瘤的持续性

John T Keane¹, David A Degaramo¹, Heather M Sosnoski¹

¹Systems Pharmacology and Translational Therapeutics, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA 19104.

Molecular therapy : the journal of the American Society of Gene Therapy

|January 11, 2026

概括

工程化CAR T细胞分泌互白素-23 (IL-23) 显示出对固体瘤的希望. 这种细胞因子装甲增强了T细胞的持久性和有效性,可能扩大CAR T细胞治疗的应用.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
生物技术是生物技术.

背景情况:

化学抗原受体 (CAR) T细胞治疗对血液癌症有效,但由于免疫抑制性瘤微环境,在固体瘤中受到限制.
第四代CAR T细胞,或"装甲"CAR T细胞,被设计为分泌促炎细胞因子,以克服这种免疫抑制.

研究的目的:

设计和评估TnMUC1向的CAR T细胞,这些细胞构成性地分泌单链白内素-12 (scIL-12) 或单链白内素-23 (scIL-23).
在固体瘤模型中评估细胞因子装甲对CAR T细胞效应器功能,瘤生长延迟,生存,体内持久性和分化状态的影响.

主要方法:

工程TnMUC1向的CAR T细胞可以分泌scIL-12或scIL-23.
实验室内对效应器功能的评估,包括干扰素-生产和细胞毒性.
使用人类乳腺癌和前列腺癌的老鼠异种移植模型进行体内评估.

主要成果:

与非装甲细胞相比,scIL-12和scIL-23装甲的CAR T细胞在体外表现出增强的效应器功能.
分泌scIL-12或scIL-23的CAR T细胞显著延迟了瘤生长,并在体内延长了生存时间.
scIL-23分泌显著增加了CAR T细胞在体内持久性,并保持了早期分化状态.

结论:

CAR-T细胞对scIL-12或scIL-23的构成性分泌增强了它们对固体瘤的抗瘤活性.
scIL-23装甲是一种有前途的策略,可以改善固体瘤中CAR T细胞的持久性和有效性,从而有可能扩大治疗应用.

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