肿瘤微环境（TME）是一个动态而复杂的系统，其网络结构不断变化，特别是影响氧化还原稳态。这些改变共同塑造了一个多样化的生态系统，通过影响 TME 的细胞和分子成分，积极支持肿瘤进展。尽管癌症免疫疗法在临床上取得了显着的进步，但其临床应用范围受到 TME 改变和肿瘤免疫原性不足的限制。最近的研究表明，即使对于免疫原性较低的实体瘤患者，一些常规和靶向治疗策略也可以增强免疫治疗的疗效。这些策略通过损伤相关分子模式 (DAMP) 的 ROS 依赖性释放来引发免疫原性细胞死亡 (ICD)。这些 DAMP 识别并与免疫细胞上的模式识别受体 (PRR) 结合，激活并成熟防御细胞，最终产生强大的抗肿瘤免疫反应。本综述强调了氧化还原稳态在协调 TME 从冷表型向热表型转变以及 ROS-ICD 轴在免疫反应诱导中的关键作用。此外，它还提供了有关利用 ROS 生成诱导 ICD 的策略的最新见解。综合分析旨在针对免疫原性较低的肿瘤开发基于 ROS 的有效癌症免疫疗法。版权所有 © 2024 Elsevier B.V. 保留所有权利。

The tumor microenvironment (TME) is a dynamic and complex system that undergoes continuous changes in its network architecture, notably affecting redox homeostasis. These alterations collectively shape a diverse ecosystem actively supporting tumor progression by influencing the cellular and molecular components of the TME. Despite the remarkable clinical advancements in cancer immunotherapy, its spectrum of clinical utility is limited by the altered TME and inadequate tumor immunogenicity. Recent studies have revealed that some conventional and targeted therapy strategies can augment the efficacy of immunotherapy even in patients with less immunogenic solid tumors. These strategies provoke immunogenic cell death (ICD) through the ROS-dependent liberation of damage-associated molecular patterns (DAMPs). These DAMPs recognize and bind with Pattern Recognition Receptors (PRRs) on immune cells, activating and maturing defense cells, ultimately leading to a robust antitumor immune response. The present review underscores the pivotal role of redox homeostasis in orchestrating the transition of TME from a cold to a hot phenotype and the ROS-ICD axis in immune response induction. Additionally, it provides up-to-date insights into strategies that leverage ROS generation to induce ICD. The comprehensive analysis aims to develop ROS-based effective cancer immunotherapies for less immunogenic tumors.Copyright © 2024 Elsevier B.V. All rights reserved.