本研究旨在阐明干扰素信号通路对肿瘤细胞铁死亡影响的机制及其与 CD8  T 细胞耗竭的相关性。研究人员利用小鼠模型和单细胞测序研究了CD8  T细胞与干扰素信号通路之间的相互作用。差异基因分析揭示了参与CD8  T细胞耗竭的关键基因，并利用生物信息学工具探索了其下游因素。利用TCGA数据库的数据分析与铁死亡相关的干扰素相关基因的表达水平，并确定其与肿瘤组织铁死亡和患者预后的相关性。进行体外实验来测量 IFN-γ、MDA 和 LPO 的水平以及肿瘤细胞活力和凋亡。使用小鼠肿瘤模型进行的体内验证证实了体外实验获得的结果，强调了沉默 HSPA6 或 DNAJB1 在增强 PD-1 治疗功效和抑制肿瘤生长和迁移方面的潜力。© 2024。作者。

This study sought to elucidate the mechanisms underlying the impact of the interferon signaling pathway on Ferroptosis in tumor cells and its correlation with CD8 + T cell exhaustion. Using mouse models and single-cell sequencing, the researchers studied the interaction between CD8 + T cells and the interferon signaling pathway. Differential gene analysis revealed key genes involved in CD8 + T cell exhaustion, and their downstream factors were explored using bioinformatics tools. The expression levels of interferon-related genes associated with Ferroptosis were analyzed using data from the TCGA database, and their relevance to tumor tissue Ferroptosis and patients' prognosis was determined. In vitro experiments were conducted to measure the levels of IFN-γ, MDA, and LPO, as well as tumor cell viability and apoptosis. In vivo validation using a mouse tumor model confirmed the results obtained from the in vitro experiments, highlighting the potential of silencing HSPA6 or DNAJB1 in enhancing the efficacy of PD-1 therapy and inhibiting tumor growth and migration.© 2024. The Author(s).