CD81 通过阻断 CD274/PD-L1 的选择性自噬降解驱动放射抵抗性胶质母细胞瘤的免疫逃逸
CD81 drives immune evasion in radioresistant glioblastoma by blocking selective autophagic degradation of CD274/PD-L1.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
胶质瘤溶瘤病毒治疗中的免疫抑制细胞：挑战与解决方案
英文原题：Immunosuppressive cells in oncolytic virotherapy for glioma: challenges and solutions.
查看英文原题
Immunosuppressive cells in oncolytic virotherapy for glioma: challenges and solutions.
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中文摘要
胶质母细胞瘤是一种高度侵袭性的脑癌，其特征是肿瘤微环境中髓系细胞大量存在。肿瘤相关巨噬细胞和小胶质细胞（TAM）以及髓源性抑制细胞（MDSCs）在促进免疫抑制和肿瘤进展中发挥关键作用。溶瘤病毒（OVs）是一种自我扩增的细胞毒性剂，能够刺激局部抗肿瘤免疫反应，并具有抑制免疫抑制性髓系细胞、招募肿瘤浸润性T淋巴细胞（TILs）至肿瘤部位的潜力，从而引发针对肿瘤的适应性免疫反应。然而，OV治疗对肿瘤驻留髓系细胞群及后续免疫反应的影响尚未完全明了。本综述概述了TAM和MDSC如何响应不同类型的OVs，以及靶向髓系细胞群以促进胶质瘤微环境中抗肿瘤免疫反应的联合治疗策略。
展开英文摘要原文
Glioblastoma is a highly aggressive form of brain cancer characterized by the abundance of myeloid lineage cells in the tumor microenvironment. Tumor-associated macrophages and microglia (TAM) and myeloid-derived suppressor cells (MDSCs), play a pivotal role in promoting immune suppression and tumor progression.
Oncolytic viruses (OVs) are self-amplifying cytotoxic agents that can stimulate local anti-tumor immune responses and have the potential to suppress immunosuppressive myeloid cells and recruit tumor-infiltrating T lymphocytes (TILs) to the tumor site, leading to an adaptive immune response against tumors.
However, the impact of OV therapy on the tumor-resident myeloid population and the subsequent immune responses are not yet fully understood. This review provides an overview of how TAM and MDSC respond to different types of OVs, and combination therapeutics that target the myeloid population to promote anti-tumor immune responses in the glioma microenvironment.
论文信息
- 作者
- Liu J、Piranlioglu R、Ye F、Shu K、Lei T、Nakashima H
- 单位
- Harvey Cushing Neuro-Oncology Laboratories, Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States.United States
- 文献类型
- 综述 · 美国 NIH 资助研究
- 期刊
- Frontiers in cellular and infection microbiology2023
- 原文标识
- PubMed 37234776 · DOI 10.3389/fcimb.2023.1141034
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