Nature子刊：邹强/李靖华/李霞/崔心刚团队揭示新型细胞死亡形式双硫死亡与抗肿瘤免疫的关联

Core Viewpoint - The discovery of a new type of cell death called disulfidptosis opens new avenues for cancer treatment, particularly through targeting SLC7A11 protein and lactate dehydrogenase B (LDHB) in tumor-infiltrating CD8⁺ T cells [1][2][11]. Group 1: Disulfidptosis Discovery - In February 2023, a team from the University of Texas MD Anderson Cancer Center identified disulfidptosis, triggered by glucose deprivation in cells with high SLC7A11 expression, which effectively inhibits tumor growth without harming normal tissues [1]. - The research indicates that disulfidptosis is driven by the abnormal accumulation of disulfides, particularly in cancer cells under glucose starvation conditions [11]. Group 2: Role of LDHB in Immune Response - A study published in June 2025 revealed that LDHB promotes disulfidptosis and exhaustion of tumor-infiltrating CD8⁺ T cells, leading to impaired anti-tumor immunity, suggesting LDHB as a potential target in cancer immunotherapy [2][6]. - The mechanism involves LDHB limiting the activity of glucose-6-phosphate dehydrogenase (G6PD) in exhausted CD8⁺ T cells, resulting in NADPH depletion and subsequent disulfidptosis-mediated cell death [6][7]. Group 3: Implications for Cancer Immunotherapy - The findings highlight the distinct roles of disulfidptosis and ferroptosis in driving CD8⁺ T cell exhaustion, indicating that targeting LDHB could be a promising therapeutic strategy in cancer immunotherapy [9]. - The research expands the understanding of disulfidptosis, showing its impact on the functionality of CD8⁺ T cells and its potential implications for enhancing anti-tumor immune responses [11].