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阻断PD-1增加了类似干细胞的CD8T细胞的自我更新,以弥补它们加速分化成效应器的差异化

Amanda L Gill¹, Peter H Wang², Judong Lee¹

¹Emory Vaccine Center and Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA 30329, USA.

Science immunology

|August 25, 2023

概括

编程死亡蛋白1 (PD-1) 阻塞疗法在慢性感染期间保持关键的干状CD8T细胞. 这种疗法增强了效应细胞的分化和增殖,保留了干状细胞池,以维持免疫力.

科学领域:

免疫学免疫学免疫学
病毒学病毒学
癌症生物学癌症生物学

背景情况:

干状CD8T细胞 (PD-1+TCF-1+) 在慢性感染和癌症期间对持续的T细胞免疫至关重要.
这些细胞是PD-1向免疫治疗后效应体CD8T细胞的来源.
检查点封锁对这些类似干细胞的祖先细胞数量的影响尚不清楚.

研究的目的:

为了确定PD-1阻断是否会在慢性病毒感染期间减少类似干细胞的CD8 T细胞群.
通过免疫疗法,研究干状CD8T细胞在免疫疗法下维持或耗尽的机制.

主要方法:

使用了一种慢性淋巴细胞胆膜炎病毒 (LCMV) 感染的小鼠模型.
向接受治疗的小鼠注射抗PD-1 (αPD-1) 或抗PD-L1 (αPD-L1) 抗体.
使用显微镜观察细胞分裂并评估细胞群和功能.

主要成果:

阻断PD-1增加了效应细胞分化和干状CD8T细胞的增殖,维持了它们的数量.
这些细胞的自我更新取决于mTOR途径.
观察到不对称的细胞分裂,产生一个差异化和一个自我更新的子细胞,保持干状池.

结论:

阻断PD-1并不会耗尽类似干细胞的CD8T细胞;相反,它促进了它们的增殖并维持了它们的数量.
干状CD8T细胞在PD-1阻断后保留了它们的功能和转录特征.
研究结果支持继续使用PD-1定向免疫疗法治疗慢性感染和癌症.

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