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免疫原性细胞死亡的溶瘤病毒治疗:肿瘤免疫治疗的利剑。

Immunogenic cell death-based oncolytic virus therapy: A sharp sword of tumor immunotherapy.

机构信息

The First Clinical College of Wenzhou Medical University, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.

Wenzhou Key Laboratory of Cancer-related Pathogens and Immunity, Experiential Center of Basic Medicine, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.

出版信息

Eur J Pharmacol. 2024 Oct 15;981:176913. doi: 10.1016/j.ejphar.2024.176913. Epub 2024 Aug 16.

DOI:10.1016/j.ejphar.2024.176913
PMID:39154830
Abstract

Tumor immunotherapy, especially immune checkpoint inhibitors (ICIs), has been applied in clinical practice, but low response to immune therapies remains a thorny issue. Oncolytic viruses (OVs) are considered promising for cancer treatment because they can selectively target and destroy tumor cells followed by spreading to nearby tumor tissues for a new round of infection. Immunogenic cell death (ICD), which is the major mechanism of OVs' anticancer effects, is induced by endoplasmic reticulum stress and reactive oxygen species overload after virus infection. Subsequent release of specific damage-associated molecular patterns (DAMPs) from different types of tumor cells can transform the tumor microenvironment from "cold" to "hot". In this paper, we broadly define ICD as those types of cell death that is immunogenic, and describe their signaling pathways respectively. Focusing on ICD, we also elucidate the advantages and disadvantages of recent combination therapies and their future prospects.

摘要

肿瘤免疫疗法,特别是免疫检查点抑制剂(ICIs),已应用于临床实践,但免疫治疗反应率低仍然是一个棘手的问题。溶瘤病毒(OVs)被认为是癌症治疗的有前途的方法,因为它们可以选择性地靶向和破坏肿瘤细胞,然后传播到附近的肿瘤组织进行新一轮的感染。免疫原性细胞死亡(ICD)是 OVs 抗癌作用的主要机制,是由病毒感染后内质网应激和活性氧超负荷引起的。不同类型的肿瘤细胞随后从特定损伤相关分子模式(DAMPs)的释放可以将肿瘤微环境从“冷”转变为“热”。在本文中,我们将 ICD 广泛定义为那些具有免疫原性的细胞死亡类型,并分别描述它们的信号通路。聚焦于 ICD,我们还阐明了最近联合治疗的优缺点及其未来前景。

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Immunogenic cell death-based oncolytic virus therapy: A sharp sword of tumor immunotherapy.免疫原性细胞死亡的溶瘤病毒治疗:肿瘤免疫治疗的利剑。
Eur J Pharmacol. 2024 Oct 15;981:176913. doi: 10.1016/j.ejphar.2024.176913. Epub 2024 Aug 16.
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