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
武装 NK 细胞用于实体瘤免疫治疗
英文原题：Weaponizing natural killer cells for solid cancer immunotherapy.
查看英文原题
Weaponizing natural killer cells for solid cancer immunotherapy.
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中文摘要
增强自然杀伤（NK）细胞介导的固有免疫已成为治疗难治性实体瘤的一种有前景的免疫治疗策略。单克隆抗体（mAb）治疗已被用于激活NK细胞介导的针对实体瘤的抗体依赖性细胞毒性（ADCC）。然而，癌细胞可利用多种免疫抑制机制逃避免疫监视，这可能削弱NK细胞的ADCC。目前可利用安全增强NK细胞ADCC的机制，例如通过暂时抑制受体内吞作用来增加抗体从靶细胞向效应细胞的呈递，从而增强NK细胞介导的针对实体瘤的ADCC。本综述总结并讨论了该领域的最新进展，并强调了当前及未来潜在利用免疫疗法以最大化固有抗癌免疫治疗疗效的方向。
展开英文摘要原文
Enhancing natural killer (NK) cell-based innate immunity has become a promising strategy for immunotherapy against hard-to-cure solid cancers. Monoclonal antibody (mAb) therapy has been used to activate NK-cell-mediated antibody-dependent cellular cytotoxicity (ADCC) towards solid cancers. Cancer cells, however, can subvert immunosurveillance using multiple immunosuppressive mechanisms, which may hamper NK cell ADCC.
Mechanisms to safely enhance ADCC by NK cells, such as utilizing temporary inhibition of receptor endocytosis to increase antibody presentation from target to effector cells can now be used to enhance NK-cell-mediated ADCC against solid tumors. This review summarizes and discusses the recent advances in the field and highlights current and potential future use of immunotherapies to maximize the therapeutic efficacy of innate anticancer immunity.
论文信息
- 作者
- Wong JKM、Dolcetti R、Rhee H、Simpson F、Souza-Fonseca-Guimaraes F
- 第一作者单位
- The University of Queensland Diamantina Institute, The University of Queensland, Woolloongabba, QLD 4102, Australia.Australia
- 通讯作者单位
- The University of Queensland Diamantina Institute, The University of Queensland, Woolloongabba, QLD 4102, Australia. Electronic address: f.guimaraes@uq.edu.au.Australia
- 文献类型
- 综述 · 美国政府（非公共卫生署）资助研究 · 非美国政府资助研究
- 期刊
- Trends in cancer2023 Feb
- 原文标识
- PubMed 36379852 · DOI 10.1016/j.trecan.2022.10.009