RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
CD155-TIGIT 轴作为癌症免疫治疗的治疗靶点
英文原题：CD155-TIGIT Axis as a Therapeutic Target for Cancer Immunotherapy.
查看英文原题
CD155-TIGIT Axis as a Therapeutic Target for Cancer Immunotherapy.
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中文摘要
免疫检查点抑制剂（ICIs）在治疗许多晚期癌症方面显示出前所未有的疗效。尽管FDA批准的ICIs在治疗许多晚期癌症方面显示出有前景的疗效，但其应用受到低缓解率、免疫相关不良事件（irAE）和耐药性的极大限制。开发新型ICIs在改善晚期癌症患者的生存和预后方面具有巨大前景。T细胞免疫球蛋白和ITIM结构域（TIGIT）是一种表达于T细胞、自然杀伤（NK）细胞和T调节细胞上的抑制性受体。越来越多的报道表明，阻断CD155-TIGIT轴可以激活免疫系统并恢复抗肿瘤免疫应答。本综述简要总结了TIGIT在肿瘤免疫逃逸中的作用以及靶向CD155-TIGIT轴的药物在癌症免疫治疗中的临床前和临床试验。
展开英文摘要原文
Immune checkpoint inhibitors (ICIs) have shown unprecedented efficacy in treating many advanced cancers. Although FDA-approved ICIs have shown promising efficacy in treating many advanced cancers, their application is greatly limited by the low response rate, immune-related adverse events (irAE), and drug resistance. Developing novel ICIs holds great promise to improve the survival and prognosis of advanced cancer patients.
T-Cell immunoglobulin and ITIM domain (TIGIT) is an inhibitory receptor expressed on T cells, natural killer (NK) cells, and T regulatory cells. Increasing reports have shown that the disrupting CD155-TIGIT axis could activate the immune system and restore antitumor immune response. This review briefly summarized the role of TIGIT in tumor immune escape and targeting CD155-TIGIT axis drugs in preclinical and clinical trials for cancer immunotherapy.
论文信息
- 作者
- Mu Y、Guan X
- 单位
- Department of Basic Medicine, School of Medicine, Taizhou University, Taizhoum, 318000, Zhejiang Province, China.China
- 文献类型
- 综述
- 期刊
- Current medicinal chemistry2024
- 原文标识
- PubMed 38666504 · DOI 10.2174/0929867330666230324152532