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
英文原题:Tumor-derived extracellular vesicles modulate innate immune responses to affect tumor progression.
Tumor-derived extracellular vesicles modulate innate immune responses to affect tumor progression.
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免疫细胞能够在肿瘤微环境(TME)中影响肿瘤进展。同时,肿瘤调节免疫细胞功能的一种机制是通过细胞外囊泡(EVs),这是一种细胞来源的细胞外膜囊泡。EVs可以作为细胞间通讯的介质,并能在细胞之间传递核酸、蛋白质、脂质和其他信号分子。近年来,研究发现EVs在肿瘤细胞与免疫细胞之间的通讯中发挥关键作用。先天免疫是免疫系统对抗肿瘤进展的第一道反应。因此,调节先天免疫细胞功能变化的肿瘤细胞来源EVs(TDEVs)在肿瘤进展中发挥重要功能。新出现的证据表明,TDEVs通过多种途径双重增强或抑制先天免疫。本综述旨在总结TDEVs对巨噬细胞、树突状细胞、中性粒细胞和NK 细胞的影响。我们还总结了它们对肿瘤进展的进一步影响,这可能为开发靶向EVs的新型肿瘤疗法提供新思路。
Immune cells are capable of influencing tumor progression in the tumor microenvironment (TME). Meanwhile, one mechanism by which tumor modulate immune cells function is through extracellular vesicles (EVs), which are cell-derived extracellular membrane vesicles.
EVs can act as mediators of intercellular communication and can deliver nucleic acids, proteins, lipids, and other signaling molecules between cells. In recent years, studies have found that EVs play a crucial role in the communication between tumor cells and immune cells. Innate immunity is the first-line response of the immune system against tumor progression.
Therefore, tumor cell-derived EVs (TDEVs) which modulate the functional change of innate immune cells serve important functions in the context of tumor progression. Emerging evidence has shown that TDEVs dually enhance or suppress innate immunity through various pathways. This review aims to summarize the influence of TDEVs on macrophages, dendritic cells, neutrophils, and natural killer cells.
We also summarize their further effects on the progression of tumors, which may provide new ideas for developing novel tumor therapies targeting EVs.
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