Xia Xueli, Wu Haisheng, Chen Yuxuan, Peng Huiyong, Wang Shengjun
Department of Laboratory Medicine, Jiangsu Province Engineering Research Center for Precise Diagnosis and Treatment of Inflammatory Diseases, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Department of Immunology, Jiangsu University School of Medicine, Zhenjiang, China.
Clin Transl Med. 2025 Mar;15(3):e70253. doi: 10.1002/ctm2.70253.
Ferroptosis is an innovative concept defined as a distinct programmed cell death mode regulated by iron-dependent lipid peroxidation accumulation. This process is governed by numerous energy metabolites such as fatty acids, amino acids and glucose, as well as iron homeostasis. In recent years, increasing studies have been devoted to the crucial effects of ferroptosis in immune cells during the pathogenesis of diseases such as infections, tumours and autoimmune disorders. This review summarises the latest advancements in T-cell ferroptosis, addresses the key components and mechanism of ferroptosis in T cells during inflammatory conditions and tumour progression, and highlights the potential target for treating related diseases. KEY POINTS: Ferroptosis-related mechanisms significantly affect the biology of CD4 T-cell subsets and are further involved in inflammatory diseases. Crosstalk between CD8 T cells and tumour cells induces ferroptosis in the tumour microenvironment. Glutathione peroxidase 4 loss promotes regulatory T-cell ferroptosis to enhance anti-tumour immunity.
铁死亡是一个创新概念，被定义为一种由铁依赖性脂质过氧化积累调节的独特程序性细胞死亡模式。这一过程受多种能量代谢物如脂肪酸、氨基酸和葡萄糖以及铁稳态的调控。近年来，越来越多的研究致力于探讨铁死亡在感染、肿瘤和自身免疫性疾病等发病机制中对免疫细胞的关键作用。本综述总结了T细胞铁死亡的最新进展，阐述了炎症状态和肿瘤进展过程中T细胞铁死亡的关键成分和机制，并强调了治疗相关疾病的潜在靶点。要点：铁死亡相关机制显著影响CD4 T细胞亚群的生物学特性，并进一步参与炎症性疾病。CD8 T细胞与肿瘤细胞之间的相互作用在肿瘤微环境中诱导铁死亡。谷胱甘肽过氧化物酶4缺失促进调节性T细胞铁死亡以增强抗肿瘤免疫力。
