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
肿瘤微环境中的 NK 细胞耗竭
英文原题：NK cell exhaustion in the tumor microenvironment.
查看英文原题
NK cell exhaustion in the tumor microenvironment.
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中文摘要
自然杀伤（NK）细胞通过死亡受体和细胞毒性颗粒杀死突变细胞，在控制癌症进展中发挥重要作用。然而，在肿瘤微环境（TME）中，NK细胞经常表现出耗竭状态，这损害了它们的免疫监视功能并促进肿瘤免疫逃逸。新兴研究正在不断揭示TME中NK细胞耗竭的特性和机制。在这篇综述中，我们将简要介绍NK细胞的成熟、定位、稳态和细胞毒性。然后，我们将从四个方面总结目前对TME中NK细胞耗竭主要机制的理解：抑制性和激活性信号失调、肿瘤细胞来源因子、免疫抑制细胞，以及代谢与耗竭。我们还将讨论目前正在开发的用于逆转NK细胞耗竭并增强TME中NK细胞细胞毒性的治疗策略。
展开英文摘要原文
Natural killer (NK) cells kill mutant cells through death receptors and cytotoxic granules, playing an essential role in controlling cancer progression.
However, in the tumor microenvironment (TME), NK cells frequently exhibit an exhausted status, which impairs their immunosurveillance function and contributes to tumor immune evasion. Emerging studies are ongoing to reveal the properties and mechanisms of NK cell exhaustion in the TME. In this review, we will briefly introduce the maturation, localization, homeostasis, and cytotoxicity of NK cells.
We will then summarize the current understanding of the main mechanisms underlying NK cell exhaustion in the TME in four aspects: dysregulation of inhibitory and activating signaling, tumor cell-derived factors, immunosuppressive cells, and metabolism and exhaustion.
We will also discuss the therapeutic approaches currently being developed to reverse NK cell exhaustion and enhance NK cell cytotoxicity in the TME.
论文信息
- 作者
- Jia H、Yang H、Xiong H、Luo KQ
- 单位
- Faculty of Health Sciences, University of Macau, Taipa, Macao SAR, China.China
- 文献类型
- 综述 · 非美国政府资助研究
- 期刊
- Frontiers in immunology2023
- 原文标识
- PubMed 38022646 · DOI 10.3389/fimmu.2023.1303605
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