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通过APOBEC3s介导的突变性重编程瘤免疫:从基因组不稳定到免疫检查点相互作用

Qiaoxi Li^1,2, Wenyu Wan^1,2, Zihan Zhu^1,2

¹Department of Dermatology, The First Hospital of China Medical University, Shenyang, China.

Frontiers in immunology

|February 27, 2026

概括

在阿波利波蛋白B mRNA编辑催化多类3 (APOBEC3) 子家族驱动癌症突变和基因组不稳定. 根据癌症背景,APOBEC3s可以增强抗瘤免疫力或促进免疫逃避.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
遗传学是一个遗传学.

背景情况:

最初以抗病毒防御而闻名的阿波利波蛋白B mRNA编辑催化型多类 (APOBEC) 家族,现在被认为是癌症体质突变的关键来源.
APOBEC3亚家族 (APOBEC3s),特别是APOBEC3A和APOBEC3B,对基因组的不稳定性,克隆进化和瘤的治疗适应性作出了重大贡献.

研究的目的:

审查癌症中APOBEC3家族的免疫格局和生物化学特征.
探索APOBEC3活性在塑造抗瘤免疫力和影响治疗反应方面的双重作用.
讨论APOBEC3介导的突变发生对癌症免疫编辑和免疫检查点路径的影响.

主要方法:

在癌症中对APOBEC3酶进行现有研究的文献综述和综合.
分析APOBEC3诱导突变对瘤突变负担和新抗原形成的影响.
检查APOBEC3活性,免疫信号和固体瘤中的免疫逃避之间的关系.

主要成果:

APOBEC3s促进基因组的不稳定性,并可以通过增加新抗原和T细胞透来增强抗瘤免疫力.
持续的APOBEC3激活还可以通过慢性炎症和PD-1/PD-L1信号传递导致免疫抑制,导致T细胞功能障碍和对免疫治疗的抵抗.
APOBEC3活性对抗瘤免疫的净效应取决于情境,影响免疫编辑和治疗结果.

结论:

在固体瘤中,APOBEC3介导的突变发生是基因组不稳定性和瘤免疫交叉之间的关键联系.
调节APOBEC3活动是一个潜在的治疗策略,但由于其在免疫中的双重作用,需要依赖于上下文的方法.
了解APOBEC3s,基因组不稳定性和瘤免疫微环境之间的复杂关系对于开发有效的癌症治疗是至关重要的.

关键词:

在APOBEC3中,我们使用了cytidine deaminases.基因组不稳定性和DNA修复免疫检查点封锁封锁突变的签名突变的签名新抗原和免疫治疗耐药性的新抗原.精确免疫瘤学精确免疫瘤学瘤免疫的微环境瘤免疫编辑免疫编辑

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