免疫原性细胞死亡
免疫系统
肿瘤微环境
癌症研究
免疫疗法
活性氧
氧化应激
免疫
化学
体内
细胞毒性T细胞
光热治疗
程序性细胞死亡
双金属片
癌细胞
炎症
抗原
血管生成
免疫检查点
获得性免疫系统
细胞生物学
过氧化物酶
谷胱甘肽
T细胞
谷胱甘肽过氧化物酶
癌症
体外
细胞内
细胞
抗氧化剂
作者
Yanbing Huang,Lei Ding,Yanbing Cao,Qiang Feng,Yanjuan Li,Jianmin Wang,Zhixiong Cai,Fuli Xin,Peiyuan Wang,Jingfeng Liu
标识
DOI:10.1002/advs.202512578
摘要
Treating hepatocellular carcinoma (HCC) remains a significant clinical challenge because of its immunosuppressive tumor microenvironment (TME) and poor response to immunotherapy. Immunogenic cell death (ICD) has emerged as a promising strategy for enhancing antitumor immunity through the release of tumor-associated antigens (TAAs) and damage-associated molecular patterns (DAMPs). However, efficient ICD induction requires precise regulation of oxidative stress, which is hindered by the robust antioxidant defenses of tumors, particularly glutathione (GSH)-mediated reactive oxygen species (ROS) scavenging. To address this, a platinum-cobalt (Pt/Co) bimetallic nanozyme (BNzyme) with a mesoporous structure is developed, which exhibited enzymatic activities similar to those of peroxidase (POD) and glutathione peroxidase (GPx). The Pt/Co BNzyme not only catalyzed H2O2 to generate cytotoxic ROS but also simultaneously depleted GSH, amplifying oxidative stress and inducing tumor cell apoptosis. Additionally, near-infrared laser irradiation enhanced its enzymatic activity through mild photothermal effects, further promoting ICD. In vivo and in vitro experiments demonstrated that the Pt/Co BNzyme effectively remodeled the immune TME by increasing TAAs and dendritic-cell maturation. When combined with immune checkpoint inhibitors, this approach triggered robust systemic antitumor immunity and immune memory, effectively suppressing tumor growth and metastasis. The Pt/Co BNzyme exhibits excellent biosafety, offering a novel strategy for HCC immunotherapy.
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