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
英文原题:Tumor infiltrating lymphocytes in glioblastoma: immunobiology and translational implications.
Tumor infiltrating lymphocytes in glioblastoma: immunobiology and translational implications.
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胶质母细胞瘤(GBM)由于其低肿瘤突变负荷、深刻的抗原异质性和高度免疫抑制的微环境,给免疫治疗带来了独特的挑战。人类 GBM 中TIL(肿瘤浸润淋巴细胞)的观察结果与同源原位鼠模型中的不同:虽然几种广泛使用的鼠神经胶质瘤模型中的 TIL 显示出大量耗尽的 T 细胞,但患者肿瘤中富含功能不确定的克隆扩增的颗粒酶 K T 细胞。我们回顾了目前对 GBM 中脑肿瘤免疫周期的理解,强调了 TIL 生物学的转化意义,并评估了新兴的基于 TCR 的方法,包括过继性 TIL 转移、新抗原疫苗和工程化受体。专注于识别和利用肿瘤选择性 T 细胞可能会为 GBM 提供更合理、个性化的免疫疗法。
Glioblastoma (GBM) poses unique challenges to immunotherapy, owing to its low tumor mutational burden, profound antigenic heterogeneity, and highly immunosuppressive microenvironment. Observations of tumor-infiltrating lymphocytes (TILs) in human GBM differ from those in syngeneic orthotopic murine models: whereas TILs in several widely used murine glioma models display an abundance of exhausted T cells, patient tumors are enriched for clonally expanded granzyme K T cells of uncertain function.
We review the current understanding of the brain tumor immunity cycle in GBM, highlight the translational implications of TIL biology, and evaluate emerging TCR-based approaches, including adoptive TILs transfer, neoantigen vaccines, and engineered receptors. A refined focus on identifying and harnessing tumor-selective T cells may enable more rational, personalized immunotherapies for GBM.
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