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:Enhancing T cell infiltration in glioblastoma: a review article on challenges and therapeutic strategies.
Enhancing T cell infiltration in glioblastoma: a review article on challenges and therapeutic strategies.
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本综述重点关注如何增强T细胞浸润胶质母细胞瘤(GBM),同时克服其免疫抑制性肿瘤微环境(TME)。关键策略包括靶向髓源性抑制细胞(MDSC)以减轻免疫抑制,以及将肿瘤相关巨噬细胞(TAM)从免疫抑制性M2表型重新极化为促炎M1表型,从而增强T细胞功能。给予趋化因子有助于吸引更多效应T细胞到达肿瘤部位。免疫检查点抑制剂(ICI)与其他治疗联合可进一步提高T细胞活性。要增强GBM免疫治疗效果,还必须处理TME中的免疫抑制信号,例如转化生长因子β(TGF-β)和白细胞介素-10(IL-10)。
This review focuses on enhancing T-cell infiltration in glioblastoma (GBM) while overcoming its immunosuppressive tumor microenvironment (TME). Key strategies include targeting myeloid-derived suppressor cells (MDSCs) to reduce immunosuppression and repolarizing tumor-associated macrophages (TAMs) from an M2 (immunosuppressive) phenotype to an M1 (proinflammatory) phenotype to increase T-cell function.
Administering chemokines can help attract more effector T cells to the tumor site. Combining immune checkpoint inhibitors (ICIs) with other treatments can further increase T cell activity. To make immunotherapy more effective in GBM, it is also essential to address the immunosuppressive signals in the TME, such as transforming growth factor beta (TGF- ) and interleukin-10 (IL-10).
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