CELL INTELLIGENCE · 肿瘤细胞治疗研究

LRIG2 通过 LAMP1-STAT3 通路抑制 NK 细胞诱导的 GSDME 介导的胶质瘤细胞焦亡

LRIG2 suppresses NK cell-induced GSDME-mediated pyroptosis via the LAMP1-STAT3 pathway in glioma.

LRIG2 通过 LAMP1-STAT3 通路抑制 NK 诱导的 GSDME 介导的细胞焦亡，从而实现胶质瘤免疫逃逸。靶向该轴是增强基于 NK 细胞的胶质瘤免疫治疗的一种有前景的策略，使 LRIG2 成为潜在的生物标志物和治疗靶点。

装甲 CAR-T 细胞抗耗竭：胶质母细胞瘤的工程化策略

Armoring CAR-T Cells Against Exhaustion: Engineering Strategies for Glioblastoma.

胶质母细胞瘤过继性细胞治疗后，树突状细胞功能障碍是免疫逃逸的基础

Dendritic Cell Dysfunction Underlies Immune Escape After Adoptive Cellular Therapy in Glioblastoma.

胶质瘤内在的 MAPK/ERK 信号通路通过 T 细胞浸润和干扰素应答促进免疫治疗疗效

Glioma-intrinsic MAPK/ERK signaling promotes immunotherapy efficacy through T cell infiltration and interferon responses.

体内 CAR 免疫细胞工程：在恶性胶质瘤中的未来应用与挑战

In Vivo CAR-Based Immune Cell Engineering: Future Applications and Challenges in Malignant Glioma.

ROBO1 CAR-NK92 细胞中 Cbl-b 敲除增强其抗肿瘤疗效

Ablation of Cbl-b in ROBO1 CAR-NK92 Cells Enhances Their Antitumor Efficacy.

推进靶向蛋白降解：pLIRTAC 在胶质瘤与 CAR-T 细胞治疗中的作用

Advancing targeted protein degradation: pLIRTAC's role in glioma and CAR-T cell therapy.

异体 CAR-T 的制备可规避胶质母细胞瘤患者自体产品的功能缺陷

Generation of Allogeneic CAR-T Circumvents Functional Deficits in Patient-Derived Autologous Product for Glioblastoma.

非病毒型细胞因子诱导型含 SH2 蛋白位点特异性整合的成纤维细胞活化蛋白 α 靶向 CAR-T 细胞在胶质母细胞瘤中实现强效抗肿瘤疗效

Non-Viral Cytokine-Inducible SH2 Containing Protein Locus-Specific Integrated Fibroblast Activation Protein Alpha-Targeting Chimeric Antigen Receptor

蛋白质翻译后修饰的双重调控：NK 细胞治疗胶质母细胞瘤的瓶颈与突破

Dual Regulation of Post-Translational Modification of Proteins: Bottlenecks and Breakthroughs in NK Cell Therapy for Glioblastoma.