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.
我们的工作确立了CD81作为连接放射抵抗与免疫逃逸的关键桥梁,其通过维持GBM中CD274的丰度发挥作用,并突显CD81作为优化放射免疫治疗的有前景的治疗靶点。
英文原题:Adoptive Cell Therapies for Glioblastoma: A Quest for Cures from Within.
Adoptive Cell Therapies for Glioblastoma: A Quest for Cures from Within.
胶质母细胞瘤(GBMs)是最具侵袭性的脑癌类型,对目前的标准治疗以及能使其他癌症患者获益的免疫检查点疗法均顽固难治。
胶质母细胞瘤(GBM)是最具侵袭性的脑癌类型,对现有标准治疗以及其他癌症患者获益的免疫检查点治疗均具有耐药性。利用患者自身免疫细胞的过继细胞疗法(ACT)长期以来一直被探索作为治疗策略,包括历史上研究过的淋巴因子激活的杀伤细胞(LAK)、不断发展的嵌合抗原受体(CAR)导向免疫细胞、新兴的肿瘤浸润T淋巴细胞(TIL)疗法等。临床前和临床研究已显示出前景,但也凸显了重大挑战。在本综述中,我们总结了这些发现,重点介绍了最新进展,讨论了当前的局限性,并强调ACT如何可能从对TIL与GBM肿瘤微环境(TME)内其他细胞共同进化的当代及未来认识中获益。
Glioblastomas (GBMs) are the most aggressive form of brain cancer recalcitrant to both current standard-of-care and immune checkpoint therapies that benefit other cancer patients. Adoptive cell therapies (ACT) using patients' own immune cells have long been explored as a treatment strategy, including the historically studied lymphokine-activated killer (LAK) cells, the evolving chimeric antigen receptor (CAR) directed immune cells, the newly emerging tumor-infiltrating T lymphocyte (TIL) therapies, and others. Preclinical and clinical studies have shown promise but also highlighted significant challenges. In this review, we summarize these findings, highlight recent developments, discuss current limitations, and emphasize how ACT may benefit from contemporary and future insights into the co-evolution of TILs with other cells within the GBM tumor microenvironment (TME).
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