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:γδ T cells as critical anti-tumor immune effectors.
γδ T cells as critical anti-tumor immune effectors.
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虽然介导抗肿瘤免疫的效应细胞历来被归因于αβ T细胞和NK 细胞,但γδ T细胞现在被认为是一种介导肿瘤排斥的补充机制。γδ T细胞具有从抗原呈递到调节功能的一系列功能,并且重要的是,在其他免疫效应细胞可能失效的情况下,它们在引发抗肿瘤反应中具有关键作用。最近的发现阐明了具有特定T细胞受体和空间分布的γδ T细胞如何介导这些不同功能。它们对T细胞耗竭等功能障碍机制的相对抵抗性促进了利用γδ T细胞的治疗方法的开发,对这些细胞的进一步了解将有助于实现更有效的免疫治疗。
While the effector cells that mediate anti-tumor immunity have historically been attributed to αβ T cells and natural killer cells, γδ T cells are now being recognized as a complementary mechanism mediating tumor rejection. γδ T cells possess a host of functions ranging from antigen presentation to regulatory function and, importantly, have critical roles in eliciting anti-tumor responses where other immune effectors may be rendered ineffective.
Recent discoveries have elucidated how these differing functions are mediated by γδ T cells with specific T cell receptors and spatial distribution. Their relative resistance to mechanisms of dysfunction like T cell exhaustion has spurred the development of therapeutic approaches exploiting γδ T cells, and an improved understanding of these cells should enable more effective immunotherapies.
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