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单细胞转录组学揭示了HIV和Mycobacterium结核病共感染的病原体相互作用和T细胞重编程

Zihui Zhao^1,2, Suyue Huang^1,3, Wei Huang¹

¹Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.

Frontiers in immunology

|December 15, 2025

概括

人类免疫缺陷病毒 (HIV) 和Mycobacterium结核病 (Mtb) 的联合感染会损害免疫反应. 这项研究揭示了Th1/Th17不平衡和改变的T细胞信号作为共感染期间免疫功能障碍的关键因素.

科学领域:

免疫学免疫学免疫学
传染性疾病传染性疾病
单细胞基因组学单细胞基因组学

背景情况:

艾滋病毒和Mycobacterium tuberculosis (Mtb) 联合感染是艾滋病患者死亡的主要原因.
在共感染中,病原体相互作用和宿主免疫重塑的机制尚不清楚.

研究的目的:

用单细胞RNA测序研究未经治疗的HIV单一感染和HIV-Mtb联合感染期间的动态免疫变化.
确定关键的细胞和分子变化,有助于共同感染的免疫功能障碍.

主要方法:

单细胞RNA测序 (scRNA-seq) 在治疗前应用于来自健康对照组,HIV单一感染组和HIV-Mtb联合感染组的外周血液单核细胞 (PBMC).
使用定向环形图 (DAG) 来推断从健康状态到感染状态的伪时间轨迹.
进行细胞通信分析以评估相互作用的变化.

主要成果:

在CD8+ T细胞和单细胞中观察到TNF-α和TGF-β信号的逐渐下降,沿着健康到共感染的连续链.
Th1细胞成为抗结核作用因子,而Th17细胞表现出疲劳和核糖体应激的迹象.
同时感染导致细胞相互作用减少,但信号强度增加,T细胞从MHCII类向I类信号显著转移,涉及抑制检查点的上调.

结论:

这项研究提供了HIV-Mtb联合感染中免疫变化的单细胞解决路线图.
Th1/Th17不平衡和MHC-I偏差的T细胞信号重构被确定为恢复免疫平衡的潜在治疗标.

关键词:

艾滋病毒-Mtb同时感染 T细胞耗尽的情况这就是TNF信号传递.Th1/Th17 的不平衡.单细胞转录组学单细胞转录组学

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