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Measurement of BK-polyomavirus Non-Coding Control Region Driven Transcriptional Activity Via Flow Cytometry

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Published on: July 13, 2019

捐赠者变异性和PD-1表达极限 BK 多重瘤病毒特异性T细胞功能和疗法

Maud Wilhelm¹, Amandeep Kaur, Anne Geng

¹Transplantation and Clinical Virology, Department of Biomedicine, University of Basel, Basel, Switzerland.

Transplantation

|April 9, 2025

概括

使用G-Rex培养物优化BK多重瘤病毒特异性T细胞的ex vivo扩张,可以提高细胞数量和细胞毒性. 像 pembrolizumab 这样的免疫检查点抑制剂可以改善 T 细胞功能,并克服 BKPyV 脏病的采用细胞疗法中的供体变异性.

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科学领域:

免疫学免疫学免疫学
移植医学移植医学
细胞疗法细胞疗法

背景情况:

乙基多瘤病毒 (BKPyV) 病是造成移植失败的主要原因.
目前的治疗重点是减少免疫抑制以恢复BKPyV特异性免疫力.
活体扩展的T细胞提供了潜力,但由于捐赠者的变异性,其疗效不足于最佳.

研究的目的:

优化BKPyV特异性T细胞的体外扩张协议.
为了比较T细胞扩张的传统和G-Rex培养系统.
评估免疫检查点抑制剂对T细胞功能的影响.

主要方法:

对比BKPyV特异性T细胞的常规和G-Rex扩张培养.
刺激的T细胞与BKPyV池以及评估的细胞因子/细胞毒性反应.
评估了编程细胞死亡蛋白1 (PD-1) 和PD-1连接体1 (PD-1L) 的表达.
评估了pembrolizumab对T细胞反应和细胞毒性的影响.

主要成果:

G-Rex培养物比传统培养物产生更高的细胞数量.
扩张的T细胞显示出多功能细胞因子的产生和对BKPyV感染细胞的细胞毒性.
经G-Rex扩展的T细胞显示PD-1表达的增加.
布罗利祖马布降低了PD-1表达,增强了T细胞反应,增加了细胞毒性.

结论:

在ex vivo扩展的T细胞上升调的PD-1有助于供体变异性,并可能限制采用细胞治疗的疗效.
在炎症条件下,BKPyV感染的近管上皮细胞 (RPTEC) 在炎症条件下调节PD-L1.
免疫检查点抑制剂的ex vivo添加值得评估,以加强移植患者的BKPyV特异性T细胞治疗.