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首页> 外文期刊>Expert opinion on therapeutic targets >Targeting TLR3 with no RIG-I/MDA5 activation is effective in immunotherapy for cancer
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Targeting TLR3 with no RIG-I/MDA5 activation is effective in immunotherapy for cancer

机译：靶向未激活RIG-I / MDA5的TLR3在癌症的免疫治疗中有效

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Introduction: Many forms of RNA duplexes with agonistic activity for pattern-recognition receptors have been reported, some of which are candidates for adjuvant immunotherapy for cancer. These RNA duplexes induce cytokines, interferons (IFNs) and cellular effectors mainly via two distinct pathways, TLR3/TICAM-1 and MDA5/MAVS. Areas covered: We determined which pathway of innate immunity predominantly participates in evoking tumor immunity in response to RNA adjuvants. Expert opinion: In knockout (KO) mouse studies, robust cytokine or IFN production is dependent on systemic activation of the MAVS pathway, whereas maturation of dendritic cells (DCs) to drive cellular effectors (i.e., NK and CTL) depends on the TICAM-1 pathway in DCs. MAVS activation often causes endotoxin-like cytokinemia, while the TICAM-1 activation does not. Unlike the TLR/MyD88 pathway, this TICAM-1 pathway barely accelerates tumor progression. Although the therapeutic effect in human patients of MAVS-activating or TICAM-1-activating RNA duplexes remains undetermined, the design of a TLR3 agonist with optimized toxicity and dose is an important goal for human immunotherapy. Here we summarize current knowledge on available RNA duplex formulations, and offer a possible approach to developing a promising RNA duplex for clinical tests.
机译：简介：已经报道了多种形式的对模式识别受体具有激动活性的RNA双链体，其中一些是癌症辅助免疫疗法的候选者。这些RNA双链体主要通过两种不同的途径TLR3 / TICAM-1和MDA5 / MAVS诱导细胞因子，干扰素（IFN）和细胞效应子。涵盖的领域：我们确定了先天免疫的主要途径是响应RNA佐剂而参与引起肿瘤的免疫。专家意见：在基因敲除（KO）小鼠研究中，强大的细胞因子或IFN产生取决于MAVS途径的系统激活，而树突状细胞（DC）的成熟以驱动细胞效应子（即NK和CTL）取决于TICAM- DC中的1条路径。 MAVS激活通常会引起内毒素样细胞因子血症，而TICAM-1激活则不会。与TLR / MyD88途径不同，此TICAM-1途径几乎不能促进肿瘤进展。尽管尚未确定MAVS激活或TICAM-1激活RNA双链体在人类患者中的治疗效果，但设计具有最佳毒性和剂量的TLR3激动剂是人类免疫治疗的重要目标。在这里，我们总结了有关可用的RNA双链体制剂的当前知识，并提供了开发用于临床测试的有希望的RNA双链体的可能方法。

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