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缺氧肿瘤细胞系裂解物致敏的树突状细胞疫苗对肝细胞癌表现出更好的治疗效果

英文原题:Hypoxic tumor cell line lysate-pulsed dendritic cell vaccine exhibits better therapeutic effects on hepatocellular carcinoma.

PubMed 2025/03/07(内容时间) Br J Cancer Q1 · IF 7.8(JCR 2025)

研究概要

本研究表明缺氧HCC细胞系裂解物致敏的DC疫苗可作为HCC的一种潜在治疗策略。

研究思路结论见上方概要

树突状细胞(DC)疫苗通过触发抗原特异性抗肿瘤免疫,是一种有前景的肝细胞癌(HCC)免疫疗法。缺氧有助于肿瘤细胞中抗原表达水平更高、谱系更广。

本研究旨在比较缺氧与常氧HCC细胞系裂解物致敏DC疫苗之间的免疫活性和治疗效果。

结果显示,缺氧HCC细胞系裂解物致敏的DC疫苗在体外产生白细胞介素-12以及促进T细胞增殖和细胞毒性方面表现出更强的活性。在HCC小鼠中,缺氧HCC细胞系裂解物致敏的DC疫苗在改善生存时间和肿瘤体积、诱导瘤内细胞毒性T细胞浸润和活化以及肿瘤细胞凋亡方面显示出更好的疗效。腺苷酸激酶4衍生抗原对于缺氧HCC细胞系裂解物致敏的DC疫苗所引发的T细胞杀伤具有重要作用。

展开英文摘要原文

BACKGROUND: Dendritic cell (DC) vaccine is a promising immunotherapy for hepatocellular carcinoma (HCC) via triggering antigen-specific anti-tumor immunity. Hypoxia contributes to higher level and broader spectrum of antigen expression in tumor cells. METHODS: This study aims to compare immunological activity and therapeutic efficacy between hypoxic and normoxic HCC cell line lysate-pulsed DC vaccines. RESULTS: The results showed that hypoxic HCC cell line lysate-pulsed DC vaccines exhibited a stronger activity in producing interleukin-12 and promoting T cell proliferation and cytotoxicity in vitro. In HCC mice, hypoxic HCC cell line lysate-pulsed DC vaccines displayed a better efficacy in improving survival time and tumor volume and inducing intratumoral cytotoxic T cell infiltration and activation as well as tumor cell apoptosis. Adenylate kinase 4-derived antigens were important for hypoxic HCC cell line lysate-pulsed DC vaccine-elicited T cell killing. CONCLUSIONS: In conclusion, this study demonstrated hypoxic HCC cell line lysate-pulsed DC vaccine as a potential therapeutic strategy for HCC.

论文信息

作者
Jeng LB、Shih FY、Liao YW、Shyu WC、Teng CF
第一作者单位
Organ Transplantation Center, China Medical University Hospital, Taichung, Taiwan, ROC.China
通讯作者单位
Organ Transplantation Center, China Medical University Hospital, Taichung, Taiwan, ROC. chiaofangteng@gmail.com.China
期刊
British journal of cancer2025 May
原文标识
PubMed 40050434 · DOI 10.1038/s41416-025-02975-w