RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
肿瘤细胞逃避 NK 细胞杀伤的机制与基于 NK 细胞的肿瘤免疫治疗进展
英文原题：Mechanisms of tumor cell evasion from NK cell-mediated killing and advances in NK cell-based cancer immunotherapy.
查看英文原题
Mechanisms of tumor cell evasion from NK cell-mediated killing and advances in NK cell-based cancer immunotherapy.
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中文摘要
自然杀伤（NK）细胞是固有免疫系统的重要组成部分，能够对感染细胞和转化细胞发挥强效的细胞毒性活性。然而，肿瘤细胞演化出多种策略以逃逸NK细胞介导的免疫监视，包括调节受体-配体相互作用、分泌免疫抑制性细胞因子、代谢干扰以及诱导NK细胞耗竭。在本综述中，我们总结了肿瘤逃逸NK细胞控制的机制，并重点介绍了基于NK细胞的免疫治疗的最新进展，包括过继性NK细胞输注、免疫检查点阻断以及CAR工程化NK细胞。目前正在进行的旨在提高NK细胞持久性、浸润能力和功能韧性的努力，有望优化临床疗效。
展开英文摘要原文
Natural killer (NK) cells represent a critical component of the innate immune system, capable of exerting potent cytotoxic activity against infected and transformed cells.
However, tumor cells evolve diverse strategies to evade NK cell-mediated surveillance, including modulation of receptor-ligand interactions, secretion of immunosuppressive cytokines, metabolic disruption, and induction of NK cell exhaustion.
In this review, we summarise the mechanisms by which tumors escape NK cell control and highlight recent advances in NK cell-based immunotherapies, including adoptive NK transfer, immune checkpoint blockade, and CAR-engineered NK cells. Ongoing efforts to improve NK cell persistence, infiltration, and functional resilience hold promise for optimising clinical efficacy.
论文信息
- 作者
- Zheng R、Wang Z、Zhang B、Li Y、Gao S、Guo Y、Meng D、Mu X
- 单位
- School of Pharmaceutical Sciences & Institute of Materia Medical, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan City, 250117, China.China
- 文献类型
- 综述
- 期刊
- Pharmaceutical science advances2026 Dec
- 原文标识
- PubMed 41799416 · DOI 10.1016/j.pscia.2026.100109
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