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
异柠檬酸脱氢酶突变型胶质瘤的免疫微环境与免疫治疗进展
英文原题：Advances in Immune Microenvironment and Immunotherapy of Isocitrate Dehydrogenase Mutated Glioma.
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Advances in Immune Microenvironment and Immunotherapy of Isocitrate Dehydrogenase Mutated Glioma.
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中文摘要
肿瘤免疫微环境和免疫治疗已成为肿瘤研究的重要议题。独特的免疫微环境在异柠檬酸脱氢酶（IDH）突变型胶质瘤恶性进展中发挥关键作用。胶质瘤中的IDH突变可抑制肿瘤相关免疫系统逃避NK细胞免疫监视；同时，突变IDH可抑制经典和旁路补体通路，并通过将异柠檬酸代谢为D-2-羟基戊二酸（2-HG）直接抑制T细胞应答。IDH作为免疫治疗潜在靶点已显示具有临床相关疗效的可能性。本文总结近年来IDH突变型胶质瘤免疫抑制微环境及免疫治疗研究进展，旨在为该类肿瘤的发生、进展和治疗研究提供新思路。
展开英文摘要原文
The tumor immune microenvironment and immunotherapy have become current important tumor research concerns. The unique immune microenvironment plays a crucial role in the malignant progression of isocitrate dehydrogenase (IDH) mutant gliomas. IDH mutations in glioma can inhibit tumor-associated immune system evasion of NK cell immune surveillance. Meanwhile, mutant IDH can inhibit classical and alternative complement pathways and directly inhibit T-cell responses by metabolizing isocitrate to D-2-Hydroxyglutaric acid (2-HG).
IDH has shown clinically relevant efficacy as a potential target for immunotherapy. This article intends to summarize the research progress in the immunosuppressive microenvironment and immunotherapy of IDH-mutant glioma in recent years in an attempt to provide new ideas for the study of occurrence, progression, and treatment of IDH-mutant glioma.
论文信息
- 作者
- Yan D、Li W、Liu Q、Yang K
- 单位
- Department of Neurosurgery, The First Affiliated Hospital of Hainan Medical University, Haikou, China.China
- 文献类型
- 综述 · 非美国政府资助研究
- 期刊
- Frontiers in immunology2022
- 原文标识
- PubMed 35769466 · DOI 10.3389/fimmu.2022.914618
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