肿瘤细胞治疗研究
英文原题：Natural killer cell dysfunction in glioma: from immune evasion to immunotherapy.
Natural killer cell dysfunction in glioma: from immune evasion to immunotherapy.
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自然杀伤（NK）细胞是固有免疫的关键组成部分，无需预先致敏即具有清除肿瘤细胞的能力。
自然杀伤（NK）细胞是固有免疫的关键组成部分，具有无需预先致敏即可清除肿瘤细胞的能力。在胶质瘤，尤其是胶质母细胞瘤中，肿瘤微环境（TME）通过MHC-I过表达、分泌TGF-和IDO以及募集髓源性抑制细胞（MDSCs）发挥强效免疫抑制作用，损害NK细胞功能。新出现的证据强调了NK细胞浸润、细胞毒性以及配体-受体动态——如NKG2D、KIRs和CX3CR1+亚群——在塑造胶质瘤患者预后和治疗反应性方面的重要意义。包括通过化疗药物（硼替佐米、地西他滨）激活NK细胞、阻断抑制性受体（NKG2A、CD161）以及与免疫检查点抑制剂联合 approaches 在内的治疗策略正在积极研究中。值得注意的是，靶向EGFR、HER2、GD2和CD133的嵌合抗原受体（CAR）工程化NK细胞因其增强的特异性和相较于CAR-T 细胞更低的毒性，在临床前胶质瘤模型中显示出前景。本综述总结了NK细胞在胶质瘤免疫中的多方面作用，并强调了恢复NK细胞功能和改善临床结局的新型免疫治疗策略。
Natural killer (NK) cells, critical components of innate immunity, possess the ability to eliminate tumor cells without prior sensitization. In gliomas, particularly glioblastoma, the tumor microenvironment (TME) exerts potent immunosuppressive effects that impair NK cell function through MHC-I overexpression, secretion of TGF- and IDO, and recruitment of myeloid-derived suppressor cells (MDSCs). Emerging evidence highlights the significance of NK cell infiltration, cytotoxicity, and ligand-receptor dynamics-such as NKG2D, KIRs, and CX3CR1 + subsets-in shaping prognosis and therapeutic responsiveness in glioma patients. Therapeutic strategies including activation of NK cells via chemotherapeutics (bortezomib, decitabine), blockade of inhibitory receptors (NKG2A, CD161), and combinatorial approaches with immune checkpoint inhibitors are under active investigation. Notably, chimeric antigen receptor (CAR)-engineered NK cells targeting EGFR, HER2, GD2, and CD133 show promise in preclinical glioma models due to their enhanced specificity and reduced toxicity compared to CAR-T cells. This review summarizes the multifaceted roles of NK cells in glioma immunity and highlights novel immunotherapeutic strategies to restore NK cell function and improve clinical outcomes.
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