EPISODE · Jan 24, 2026 · 20 MIN
425-胞外GPX4通过ZP3受体抑制抗肿瘤免疫
from 聊聊Sci
这项研究揭示了铁死亡（ferroptosis）具有较弱免疫原性的分子机制，并重点探讨了GPX4蛋白与ZP3受体在其中的核心作用。研究发现，铁死亡的细胞会释放出关键的抗氧化酶GPX4，该蛋白在胞外发挥着免疫抑制分子的功能。GPX4通过与树突状细胞表面的ZP3受体结合，激活了cAMP-PRKA信号通路，进而抑制了细胞的糖酵解代谢。这种代谢限制会导致树突状细胞无法有效成熟，并产生抗炎因子IL-10，从而削弱了CD8+ T细胞的抗肿瘤免疫反应。实验证明，阻断GPX4或ZP3能够显著增强铁死亡诱导的抗肿瘤效应。此外，临床数据表明ZP3的高表达与多种癌症的预后不良以及免疫细胞浸润减少密切相关，为癌症免疫治疗提供了潜在的新靶点。References: Liu J, Cai X, Lin J, et al. Extracellular GPX4 impairs antitumor immunity via dendritic ZP3 receptors[J]. Cell, 2026.前往小宇宙评论区与主播互动
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425-胞外GPX4通过ZP3受体抑制抗肿瘤免疫
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