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微生物群诱导的塑性T细胞增强了对抗原共享瘤的免疫控制

Tariq A Najar¹, Yuan Hao^2,3, Yuhan Hao^4,5

¹Department of Cell Biology, New York University School of Medicine, New York, NY 10016, USA.

bioRxiv : the preprint server for biology

|August 26, 2024

概括

分段丝状细菌 (SFB) 殖民化对T细胞进行了原始化,增强了抗PD-1治疗对表达SFB抗原的瘤的疗效. 这种肠道微生物群诱导的免疫反应对于有效的癌症免疫疗法至关重要.

科学领域:

免疫学免疫学免疫学
微生物学微生物学
在瘤学瘤学.

背景情况:

免疫检查点封锁 (ICB) 已经改变了癌症护理,但在许多患者中缺乏有效性.
肠道微生物群显著影响免疫反应和癌症免疫治疗结果.
连接肠道细菌与ICB疗效的机制尚不清楚.

研究的目的:

为了研究肠道共生细菌,特别是细分丝状细菌 (SFB) 如何影响ICB疗效.
探索SFB诱导的T细胞反应在控制与SFB共享抗原的瘤中的作用.

主要方法:

在患有SFB抗原表达黑色素瘤的小鼠中利用了SFB殖民.
采用T细胞受体克隆系谱追踪,命运映射和-MHC四聚合物染色.
分析了SFB对抗PD-1治疗反应的影响.

主要成果:

抗PD-1疗法仅在SFB殖民小鼠中有效抑制瘤生长.
识别了SFB特异性的Th1类细胞,这些细胞起源于肠膜本身的Th17细胞.
这些细胞产生IFN-γ和TNF-α,增强CD8+细胞毒性淋巴细胞功能,控制瘤生长.

结论:

SFB殖民促进T细胞可塑性,产生效应细胞,增强ICB对抗原共享瘤的疗效.
了解微生物对T细胞反应的影响,可以为新的癌症免疫疗法策略提供信息.

关键词:

癌症免疫学癌症免疫学自体免疫性是一种自身免疫性.细胞迁移细胞迁移分子仿真是分子仿真.粘膜免疫力粘膜免疫力瘤微环境是一个微环境.瘤排水淋巴结的淋巴结.

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