Ferroptosis is a type of regulated cell death that drives the pathophysiology of many diseases. Oxidative stress is detectable in many types of regulated cell death, but only ferroptosis involves lipid peroxidation and iron dependency. Ferroptosis originates and propagates from several organelles, including the mitochondria, endoplasmic reticulum, Golgi, and lysosomes. Recent data have revealed that immune cells can both induce and undergo ferroptosis. A mechanistic understanding of how ferroptosis regulates immunity is critical to understanding how ferroptosis controls immune responses and how this is dysregulated in disease. Translationally, more work is needed to produce ferroptosis-modulating immunotherapeutics. This review focuses on the role of ferroptosis in immune-related diseases, including infection, autoimmune diseases, and cancer. We discuss how ferroptosis is regulated in immunity, how this regulation contributes to disease pathogenesis, and how targeting ferroptosis may lead to novel therapies.

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消除铁死亡在免疫中的作用


铁死亡是一种受调节的细胞死亡，驱动许多疾病的病理生理学。在许多类型的受调节细胞死亡中都可以检测到氧化应激，但只有铁死亡涉及脂质过氧化和铁依赖性。铁死亡起源并传播自多种细胞器，包括线粒体、内质网、高尔基体和溶酶体。最近的数据表明，免疫细胞既可以诱导铁死亡，也可以发生铁死亡。从机制上理解铁死亡如何调节免疫对于理解铁死亡如何控制免疫反应以及免疫反应如何在疾病中失调至关重要。从转化上讲，需要更多的工作来生产调节铁死亡的免疫治疗药物。本综述重点关注铁死亡在免疫相关疾病中的作用，包括感染、自身免疫性疾病和癌症。我们讨论铁死亡如何在免疫中受到调节，这种调节如何促进疾病发病机制，以及针对铁死亡如何可能带来新的疗法。