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:Mesenchymal stem cells and natural killer cells interaction mechanisms and potential clinical applications.
Mesenchymal stem cells and natural killer cells interaction mechanisms and potential clinical applications.
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NK 细胞(NK细胞)是先天免疫细胞,被激活后可以对抗肿瘤细胞和病毒感染细胞。NK细胞在移植物抗白血病反应中也发挥重要作用。然而,它们可以通过分泌炎性细胞因子和增加Th1分化而过度发展炎症反应,最终导致组织损伤。如今,研究人员已将一些自身免疫性疾病和GVHD归因于NK细胞。另一方面,已表明间充质干细胞(MSCs)可以调节NK细胞的活性,而一些研究人员表明NK细胞可以导致MSCs裂解。因此,我们认为有必要研究这两种细胞及其相互接触时的信号通路,以及它们的临床应用。
Natural killer cells (NK cells) are innate immune cells that are activated to fight tumor cells and virus-infected cells. NK cells also play an important role in the graft versus leukemia response.
However, they can over-develop inflammatory reactions by secreting inflammatory cytokines and increasing Th1 differentiation, eventually leading to tissue damage. Today, researchers have attributed some autoimmune diseases and GVHD to NK cells. On the other hand, it has been shown that mesenchymal stem cells (MSCs) can modulate the activity of NK cells, while some researchers have shown that NK cells can cause MSCs to lysis.
Therefore, we considered it is necessary to investigate the effect of these two cells and their signaling pathway in contact with each other, also their clinical applications.
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