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
NK 细胞从不孤单：肿瘤微环境中的串扰与通讯
英文原题：NK cells are never alone: crosstalk and communication in tumour microenvironments.
查看英文原题
NK cells are never alone: crosstalk and communication in tumour microenvironments.
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中文摘要
免疫逃逸是癌症的一个标志。动态且异质的肿瘤微环境（TME）导致自然杀伤（NK）细胞免疫疗法的浸润不足和疗效不佳，这成为触发肿瘤进展的关键因素。理解NK细胞与TME之间的串扰为优化基于NK细胞的免疫疗法提供了新的见解。在此，我们介绍了NK细胞与9种特化TME之间直接或间接串扰的新进展，包括免疫、代谢、神经支配生态位、机械和微生物微环境，总结了TME介导的NK细胞功能抑制机制，并强调了针对NK-TME串扰的潜在靶向治疗。重要的是，我们讨论了克服抑制性TME的新策略，并为未来提供了有吸引力的展望。
展开英文摘要原文
Immune escape is a hallmark of cancer. The dynamic and heterogeneous tumour microenvironment (TME) causes insufficient infiltration and poor efficacy of natural killer (NK) cell-based immunotherapy, which becomes a key factor triggering tumour progression. Understanding the crosstalk between NK cells and the TME provides new insights for optimising NK cell-based immunotherapy.
Here, we present new advances in direct or indirect crosstalk between NK cells and 9 specialised TMEs, including immune, metabolic, innervated niche, mechanical, and microbial microenvironments, summarise TME-mediated mechanisms of NK cell function inhibition, and highlight potential targeted therapies for NK-TME crosstalk.
Importantly, we discuss novel strategies to overcome the inhibitory TME and provide an attractive outlook for the future.
论文信息
- 作者
- Zhou Y、Cheng L、Liu L、Li X
- 第一作者单位
- The First School of Clinical Medicine, Lanzhou University, 222 Tianshui South Road, Lanzhou, 730000, China.China
- 通讯作者单位
- The First School of Clinical Medicine, Lanzhou University, 222 Tianshui South Road, Lanzhou, 730000, China. lxdr21@126.com.China
- 文献类型
- 综述 · 非美国政府资助研究
- 期刊
- Molecular cancer2023 Feb 16
- 原文标识
- PubMed 36797782 · DOI 10.1186/s12943-023-01737-7
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