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TLR3 agonists and proinflammatory antitumor activities

机译：TLR3激动剂和促炎抗肿瘤活性

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Although tumor growth leads to inflammatory responses, the immune system develops tolerance to cancer. One way to break host tolerance to tumors is to activate key immune effector activities. Toward this end, various adjuvants are under investigation in an effort to harness the immune system to overcome tolerance to tumor-associated self-antigens. There is enthusiasm for the use of specific ligands for toll-like receptor 3 (TLR3) that play a key role in the innate immune system. TLR3 agonists serve as immune adjuvants because they potently induce innate immune responses by activating dendritic cell (DC) maturation and inflammatory cytokine secretion. These activities facilitate the bridge between the innate and adaptive immune systems promoting the expansion of cytotoxic T lymphocytes (CTL) that destroy cancer cells. TLR3 agonists either alone or in combination with tumor antigens have shown success in terms of enhancing immune responses and eliciting antitumor activity in preclinical models. However, TLR3 agonists can also impact regulatory cells that dampen immune responses. Thus, immune strategies that utilize TLR3 agonists should consider the relative induction of suppressive as well as beneficial antitumor immune activities. Herein, we summarize the TLR3 agonists that will hopefully come to clinical fruition.
机译：尽管肿瘤的生长会导致炎症反应，但免疫系统会发展出对癌症的耐受性。打破宿主对肿瘤的耐受性的一种方法是激活关键的免疫效应子活性。为此，正在研究各种佐剂，以利用免疫系统克服对肿瘤相关自身抗原的耐受性。人们热衷于使用在先天免疫系统中起关键作用的toll样受体3（TLR3）的特定配体。 TLR3激动剂可以用作免疫佐剂，因为它们通过激活树突状细胞（DC）成熟和炎性细胞因子分泌来有效诱导先天性免疫反应。这些活动促进了先天免疫系统和适应性免疫系统之间的桥梁，从而促进了破坏癌细胞的细胞毒性T淋巴细胞（CTL）的扩增。在临床前模型中，单独或与肿瘤抗原组合的TLR3激动剂在增强免疫应答和引发抗肿瘤活性方面已显示出成功。但是，TLR3激动剂也会影响调节细胞，从而抑制免疫反应。因此，利用TLR3激动剂的免疫策略应考虑相对诱导抑制性和有益的抗肿瘤免疫活性。在此，我们总结了有望实现临床应用的TLR3激动剂。

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