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化学R23激活将巨细胞重新编程为一种不太炎症的表型,并减缓癌的进展

Margot Lavy¹, Vanessa Gauttier¹, Alison Dumont²

¹OSE Immunotherapeutics, Nantes, France.

Frontiers in immunology

|August 4, 2023

概括

用激素抗体 (αChemR23) 向ChemR23显示出对抗癌症的治疗潜力. 这种方法调节瘤相关巨细胞 (TAMs),提高生存率和减少临床前模型中的转移.

科学领域:

免疫学免疫学免疫学
在瘤学瘤学.
药理学药理学是指药理学的学科.

背景情况:

瘤相关巨细胞 (TAMs) 促进瘤生长和对治疗的抵抗.
针对TAM是癌症治疗的一个有希望的策略.
化学R23是一种参与炎症分辨的巨细胞受体.

研究的目的:

研究用激素抗体 (αChemR23) 向ChemR23的治疗潜力.
评估αChemR23对巨细胞功能和瘤进展的影响.
评估人类癌症中ChemR23表达和TAM标记物之间的相关性.

主要方法:

分化的人类巨细胞 (GM-CSF,M-CSF,TAM类) 用αChemR23.3进行治疗.
进行了转录基因,蛋白质和功能分析.
在癌症基因图谱 (TCGA) 数据集中分析了CMKLR1 (ChemR23基因) 表达式.
在活体中,αChemR23的疗效在三阴性乳腺癌模型中进行了评估.

主要成果:

αChemR23调节M-CSF和TAM类巨细胞,改变表面标记物,细胞因子分泌和免疫功能.
人类乳腺癌和间皮瘤中CMKLR1表达与TAM标记相关.
在体内治疗αChemR23增加了存活率和减少了三阴性乳腺癌模型中的转移,与TAM调节相关.

结论:

用αChemR23针对ChemR23提供了一种针对癌症的新疗法策略.
这种方法可以通过调节炎症解决途径来规避TAMs的前瘤效应.

关键词:

化学R23受体的受体激进分子的激进分子.抗体是一种抗体.癌症癌症癌症癌症癌症巨细胞是一个巨细胞.

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