CD81 通过阻断 CD274/PD-L1 的选择性自噬降解驱动放射抵抗性胶质母细胞瘤的免疫逃逸
CD81 drives immune evasion in radioresistant glioblastoma by blocking selective autophagic degradation of CD274/PD-L1.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
铁死亡在调控胶质瘤免疫格局中的新兴作用
英文原题：Emerging roles of ferroptosis in modulating the immune landscape of glial tumours.
查看英文原题
Emerging roles of ferroptosis in modulating the immune landscape of glial tumours.
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中文摘要
大脑为癌症提供了独特的环境，营养获取有限且免疫监视高度受调控。在此，我们探讨铁死亡——一种由铁介导的脂质过氧化驱动的代谢调控性细胞死亡形式——在塑造胶质瘤中免疫细胞组成和功能方面的作用。我们综述了胶质瘤微环境中调控铁死亡的细胞群体之间复杂的代谢串扰。铁死亡诱导驻留小胶质细胞的极化，并调控 CD8+ T 细胞的细胞毒性作用以及调节性 T 细胞的免疫抑制效应。我们讨论了近期发现的铁死亡驱动的免疫逃逸机制及其对肿瘤演化的影响。此外，我们分析了将铁死亡诱导剂与免疫疗法（包括免疫检查点阻断和过继性细胞疗法）联合应用时的协同机制，这些联合策略旨在诱导有效的免疫应答并实现胶质瘤的持久控制。
展开英文摘要原文
The brain offers a unique environment for cancer, with limited access to nutrients and highly regulated immune surveillance.
Here we explore the role of ferroptosis, a form of metabolically regulated cell death driven by iron-mediated lipid peroxidation, in shaping immune-cell composition and function in glial tumours.
We review the complex metabolic crosstalk between cell populations regulating ferroptosis in the glioma milieu. Ferroptosis induces polarization of resident microglia and controls the cytotoxic roles of CD8 + T cells and the immunosuppressive effects of regulatory T cells.
We discuss recently uncovered mechanisms of ferroptosis-driven immune evasion and the impact on tumour evolution.
Additionally, we analyse mechanisms of synergy in combinations incorporating ferroptosis-inducing agents and immunotherapies, including immune checkpoint blockade and adoptive cell therapies, which aim to induce effective immune responses and durable control in gliomas.
论文信息
- 作者
- Argenziano MG、Neelakantan TV、Sperring C、Adeuyan O、Higgins DMO、Bruce JN、Kim BYS、Dovas A
- 第一作者单位
- Department of Neurosurgery, Columbia University Irving Medical Center, New York, NY, USA.United States
- 通讯作者单位
- Department of Neurosurgery, Columbia University Irving Medical Center, New York, NY, USA. mbanu@stanford.edu.United States
- 文献类型
- 综述
- 期刊
- Nature cell biology2026 Jul
- 原文标识
- PubMed 42225830 · DOI 10.1038/s41556-026-01972-2