期刊
EXPERT OPINION ON THERAPEUTIC TARGETS
卷 17, 期 5, 页码 481-483出版社
INFORMA HEALTHCARE
DOI: 10.1517/14728222.2013.781585
关键词
cancer; immune suppression; immune therapy; TLR3 agonists
资金
- NCATS NIH HHS [UL1 TR000124, UL1TR000124] Funding Source: Medline
- NCI NIH HHS [P50 CA90388, R01 CA126944, R01 CA95686, P50 CA090388, R01 CA085686] Funding Source: Medline
- NIDCR NIH HHS [K23 DE021193] Funding Source: Medline
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据