Oncolytic virus-mediated reversal of impaired tumor antigen presentation.
Oncolytic virus-mediated reversal of impaired tumor antigen presentation.
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DOI：
10.3389/fonc.2014.00077
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发表时间：
2014
影响因子：
4.7
通讯作者：
Lee PW
中科院分区：
文献类型：
--
作者：
Gujar SA;Lee PW
抗肿瘤免疫可以消除现有的癌细胞，并保持对可能复发的持续监测。当肿瘤特异性T细胞被激活时，这种抗原特异性适应性反应开始。T细胞活化需要抗原呈递细胞（APC）上的两个信号：通过主要组织相容性复合体（MHC）分子的抗原呈递和共刺激。在缺乏一种或两种信号的情况下，T细胞保持失活或甚至可以变得耐受。癌细胞及其相关的微环境策略性地阻碍肿瘤抗原的加工和呈递，从而阻止抗肿瘤免疫的发展。然而，许多研究表明，推翻肿瘤相关免疫逃避机制的干预措施可以建立具有治疗潜力的抗肿瘤免疫应答。一种这样的干预是基于溶瘤病毒（OV）的抗癌疗法。在这里，我们讨论了如何OV诱导的免疫事件覆盖肿瘤相关抗原呈递损伤，并促进适当的T细胞APC相互作用。对这种现象的详细理解对于设计将通过用所需的抗肿瘤免疫应答补充其固有的溶瘤活性来增强基于OV的抗癌疗法的功效的策略是关键的。
Anti-tumor immunity can eliminate existing cancer cells and also maintain a constant surveillance against possible relapse. Such an antigen-specific adaptive response begins when tumor-specific T cells become activated. T-cell activation requires two signals on antigen presenting cells (APCs): antigen presentation through major histocombatibility complex (MHC) molecules and co-stimulation. In the absence of one or both these signals, T cells remain inactivated or can even become tolerized. Cancer cells and their associated microenvironment strategically hinder the processing and presentation of tumor antigens and consequently prevent the development of anti-tumor immunity. Many studies, however, demonstrate that interventions that over-turn tumor-associated immune evasion mechanisms can establish anti-tumor immune responses of therapeutic potential. One such intervention is oncolytic virus (OV)-based anti-cancer therapy. Here, we discuss how OV-induced immunological events override tumor-associated antigen presentation impairment and promote appropriate T cell–APC interaction. Detailed understanding of this phenomenon is pivotal for devising the strategies that will enhance the efficacy of OV-based anti-cancer therapy by complementing its inherent oncolytic activities with desired anti-tumor immune responses.