一种用于克服非小细胞肺癌治疗中抗原异质性的多靶向 CAR-T 细胞平台
A Multi-Targeting Chimeric Antigen Receptor-T Cell Platform to Overcome Antigen Heterogeneity in the Treatment of Non-Small Cell Lung Cancer.
这些发现支持采用多靶点CAR-T 策略来应对NSCLC及可能其他实体瘤中的抗原异质性。
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
FcγRIIb 缺陷通过减弱 MDSCs 的免疫抑制表型抑制肿瘤发展
英文原题：FcγRIIb deficiency inhibits tumor development by attenuating the immunosuppressive phenotype of MDSCs.
查看英文原题
FcγRIIb deficiency inhibits tumor development by attenuating the immunosuppressive phenotype of MDSCs.
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中文摘要
调节髓源性抑制细胞（MDSC）的程序化过程，对控制肿瘤生长和抗肿瘤免疫反应至关重要。本研究考察了FcγRIIb在MDSC程序化中的作用。研究发现，FcγRIIb缺失可促进MDSC分化，并增加荷瘤小鼠脾脏中MDSC的积累；同时减弱多形核（PMN）MDSC和单核细胞（M）MDSC的免疫抑制表型。FcγRIIb⁻/⁻小鼠的肿瘤生长显著低于野生型（WT）小鼠。注射B16F10/3LL细胞后，过继转移FcγRIIb⁻/⁻ MDSC亚群与转移WT MDSC亚群相比，显著延缓了肿瘤生长。FcγRIIb⁻/⁻ MDSC中可观察到NF-κB通路活化，并与免疫抑制表型减弱相关。在人MDSC中，FcγRIIb表达与肺癌进展相关。这些发现表明，FcγRIIb对MDSC的免疫抑制表型至关重要，可能成为抗肿瘤治疗的潜在靶点。
展开英文摘要原文
Regulation of myeloid-derived suppressor cell (MDSC) programming is critical for controlling tumor growth and anti-tumor immune responses. The role of FcγRIIb in MDSC programming was examined. FcγRIIb deficiency was found to promote MDSC differentiation and increase splenic MDSC accumulation in tumor-bearing mice. This deficiency also attenuated the immunosuppressive phenotype of both polymorphonuclear (PMN)-MDSCs and monocytic (M)-MDSCs.
Tumor growth in FcγRIIb -/- mice was significantly lower than in wild-type (WT) mice. Adoptive transfer of FcγRIIb -/- MDSC subsets following B16F10/3LL injection significantly delayed tumor growth compared with transfer of WT MDSC subsets. Activation of the NF-κB pathway was observed in FcγRIIb -/- MDSCs, which was associated with the diminished immunosuppressive phenotype. In human MDSCs, FcγRIIb expression was associated with the progression of lung cancer.
These findings demonstrate that FcγRIIb is crucial for the immunosuppressive phenotype of MDSCs and may serve as a potential therapeutic target for anti-tumor therapy.
论文信息
- 作者
- Chen W、Pan J、Ning X、Li D、Shen T、Cai L、Wang S、Qian L
- 第一作者单位
- Key Laboratory of the Jiangsu Higher Education Institutions for Nucleic Acid & Cell Fate Regulation (Yangzhou University), Institute of Translational Medicine, School of Medicine, Yangzhou University, Yangzhou, 225001, PR China; School of Basic Medical Sciences, Jiangsu Medical College, Yancheng, 224005, PR China.China
- 通讯作者单位
- Department of Ophthalmology, the Affiliated Hospital of Yangzhou University, Yangzhou, 225001, PR China. Electronic address: zhuxiaoyu@yzu.edu.cn.China
- 期刊
- Immunology letters2026 Aug
- 原文标识
- PubMed 41974282 · DOI 10.1016/j.imlet.2026.107177