铁死亡是一种由脂质过氧化驱动的铁依赖性细胞死亡形式，其在形态、生化和遗传学上与细胞凋亡、坏死和自噬不同。越来越多关于铁死亡在实体瘤进展、转移、治疗和治疗耐药中的重要作用的研究已发表。研究表明，铁死亡是肿瘤免疫中的一把“双刃剑”，这意味着它可能同时具有拮抗肿瘤和促进肿瘤的功能。肿瘤微环境（TME）不仅包括肿瘤细胞，还包括周围的免疫细胞、基质细胞以及细胞外基质（ECM）、细胞因子、生长因子和细胞外囊泡（EV）等非细胞成分。在肿瘤细胞生长的复杂多样的条件下，每种成分的变化可能对肿瘤的命运产生不同的影响。最近，一些研究揭示了铁死亡与 TME 中不同成分之间的相互作用。肿瘤细胞和非肿瘤细胞在肿瘤免疫中发挥双重作用，并通过铁死亡影响肿瘤进展。本文旨在基于TME总结铁死亡在肿瘤免疫中的作用，重点探讨铁死亡与TME中不同成分相互作用的机制，阐明铁死亡如何通过不同的作用发挥促进或拮抗肿瘤的作用。 TME 中的成分，并提出了铁死亡和铁死亡相关免疫疗法的免疫调节作用的几个问题。版权所有 © 2023。由 Elsevier B.V. 出版。

Ferroptosis is an iron-dependent form of cell death driven by lipid peroxidation, which is morphologically, biochemically, and genetically distinct from apoptosis, necrosis, and autophagy. Mounting studies on the essential role of ferroptosis have been published in the progression of solid tumors, metastasis, therapy, and therapy resistance. Studies showed that ferroptosis is a "double-edged sword" in tumor immunity, which means it may have both tumor-antagonizing and tumor-promoting functions. The tumor microenvironment (TME) comprises not only tumor cells but also surrounding immune cells, stromal cells, as well as noncellular components such as the extracellular matrix (ECM), cytokines, growth factors, and extracellular vesicles (EVs). In the complex and diverse condition in TME where tumor cells grow, changes in each constituent may impact tumor destiny differently. Recently, several studies have revealed the interaction between ferroptosis and different constituents in TME. Both tumor cells and nontumor cells have a dual role in tumor immunity and influence tumor progression through ferroptosis. Herein, this review aims at summarizing the role of ferroptosis in tumor immunity based on TME, focusing on the mechanisms of the interaction between the ferroptosis and the different constituents in TME, illuminating how ferroptosis plays its role in promoting or antagonizing tumors by acting with varying components in TME and proposing several questions in immunomodulatory effects of ferroptosis and ferroptosis-associated immunotherapy.Copyright © 2023. Published by Elsevier B.V.