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:The role of myeloid-derived suppressor cells in liver cancer.
The role of myeloid-derived suppressor cells in liver cancer.
分数与星级只用于站内排序 —— 不代表疗效、安全性或个人适用性。
MDSC是未成熟的髓系免疫细胞,在肝癌模型中积聚,降低效应免疫细胞活性,促进免疫逃逸和治疗耐药。MDSC的积聚抑制CTL的作用和NK细胞的杀伤效应,诱导Treg细胞的积聚,并阻断DC的抗原呈递,从而促进肝癌的进展。近年来,免疫治疗已成为晚期肝癌放化疗后的一种有价值的治疗方法。大量研究证明,靶向MDSC已成为增强肿瘤免疫的治疗靶点之一。在临床前研究模型中,靶向MDSC在单独给药和联合给药中均显示出令人鼓舞的结果。本文阐述了肝脏的免疫微环境、MDSC的功能和调控机制,以及靶向MDSC的治疗方法。我们也期望这些策略能为未来肝癌免疫治疗提供新的视角。
MDSCs are immature myeloid immune cells, which accumulate in models of liver cancer to reduce effector immune cell activity, contribute to immune escape and treatment resistance. The accumulation of MDSCs suppresses the role of CTL and the killing effects of NK cells, induces the accumulation of Treg cells, and blocks the antigen presentation of DCs, thus promoting the progression of liver cancer. Recently, immunotherapy has emerged a valuable approach following chemoradiotherapy in the therapy of advanced liver cancer.
A considerable increasing of researches had proved that targeting MDSCs has become one of the therapeutic targets to enhance tumor immunity. In preclinical study models, targeting MDSCs have shown encouraging results in both alone and in combination administration. In this paper, we elaborated immune microenvironment of the liver, function and regulatory mechanisms of MDSCs, and therapeutic approaches to target MDSCs.
We also expect these strategies to supply new views for future immunotherapy for the treatment of liver cancer.
在 PubMed 查看 → 出版商原文(DOI) 全文 PDF(PMC)· 可下载 治疗专题与资料阅读指南 资料来源与翻译说明 报告译文或资料问题 →
MEMBER ACCOUNT
登录成功会直接打开下一页。