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艾滋病毒-1 Tat 抑制了人类微质中的TREM1表达

Grant R Campbell¹, Pratima Rawat², Rachel K To²

¹Division of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, SD.

Journal of immunology (Baltimore, Md. : 1950)

|June 16, 2023

概括

艾滋病毒感染的微质细胞通过TREM1 (在髓状细胞表达的触发受体1) 抵抗细胞死亡. 抑制TREM1会导致艾滋病毒感染的微质细胞死亡,提供一种潜在的艾滋病毒治愈策略.

科学领域:

神经免疫学神经免疫学
病毒学病毒学
细胞生物学细胞生物学

背景情况:

微质细胞作为艾滋病毒的储存库.
微细胞对艾滋病毒诱导的细胞损伤具有抗性,阻碍了艾滋病毒治愈的努力.
在骨髓细胞1 (TREM1) 上表达的触发受体与巨细胞对HIV的抗性有关.

研究的目的:

为了研究TREM1在HIV感染的微质细胞对亡的抗性中的作用.
探索TREM1作为消除艾滋病毒从微质细胞中的治疗点.

主要方法:

在感染HIV的人类微质细胞中评估TREM1表达.
在HIV感染微质细胞中基因抑制TREM1.
分析了细胞死亡,病毒载量和细胞因子表达.
研究了HIV Tat通过TLR4信号通路对TREM1的调节.

主要成果:

感染艾滋病毒的微质细胞表现出TREM1表达的增加和对亡的抵抗力.
对TREM1的遗传抑制导致HIV感染的微质细胞死亡,而不会增加病毒或炎症标志物.
艾滋病毒Tat通过涉及TLR4,TICAM1,PTGS2和PGE2.2的途径对TREM1进行上调.

结论:

TREM1对于艾滋病毒感染的微质细胞的生存至关重要.
向TREM1可以诱导HIV感染微质细胞的选择性死亡.
这种方法为消除艾滋病毒提供了一个潜在的战略,而不会引起炎症.

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