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单细胞到巨细胞的分化和细胞氧化还原恒温的变化促进了特定细胞类型的HIV潜伏反应激活

Alexandra Blanco¹, Robert A Coronado¹, Neha Arun²

¹Department of Bioengineering, University of Illinois at Urbana-Champaign, Urbana, IL 61801.

Proceedings of the National Academy of Sciences of the United States of America

|April 29, 2024

概括

艾滋病毒的潜伏时间在单细胞和巨细胞之间有所不同,受细胞状态和信号通路的影响. 向氧化还原通路揭示了细胞特异性效应,影响了艾滋病毒储库根除策略.

科学领域:

免疫学免疫学免疫学
病毒学病毒学
细胞生物学细胞生物学

背景情况:

艾滋病毒潜伏期是消除艾滋病毒的主要障碍,免疫细胞类型的调控因而有所不同.
单细胞和巨细胞在艾滋病毒的持续性和传播中发挥着关键作用.
了解细胞特异性延迟机制对于开发有效疗法至关重要.

研究的目的:

研究在单细胞到巨细胞分化和两极化过程中调节HIV潜伏的机制.
探索氧化还原通路的作用,特别是氧化系统,在HIV潜伏期.
评估针对这些途径减少艾滋病毒储存库的潜力.

主要方法:

使用THP-1单细胞生成了HIV潜伏模型,并将其分化为巨细胞.
分析了在分化和两极化 (M1与M2巨细胞) 期间的HIV活性.
研究了包括Auranofin在内的硫素系统抑制剂对HIV潜伏期的影响.

主要成果:

单细胞转化为巨细胞的分化和M2巨细胞的两极分化促进了HIV的重新激活.
蛋白激酶C信号传递和环林T1上调被确定为关键调节者.
铁素系统抑制剂对艾滋病毒潜伏时间有差异的影响:在T细胞/单细胞中促进它,但通过ROS诱导的NF-κB活性在巨细胞中逆转它.

结论:

艾滋病毒潜伏调节是细胞类型特定的,这给根除带来了挑战.
巨细胞分化和两极分化显著影响病毒的活性.
向氧化还原通路,如氧化系统,提供潜在的治疗途径,但需要细胞特异的方法.

关键词:

艾滋病毒潜伏时间HIV潜伏时间延迟促进的代理商.由单细胞衍生的巨细胞.骨髓状细胞储存库骨髓状细胞储存库甲素 (thioredoxin) 是一种甲素.

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