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艾滋病毒1对CD4+T细胞的CD96进行操纵,以破坏抗病毒免疫力

Sandra Dehn¹, Rabea Burkhard¹, Johanna Leyens¹

¹Institute for Medical Virology and Epidemiology of Viral Diseases, University Hospital Tübingen, Tübingen, Germany.

Science advances

|September 5, 2025

概括

艾滋病毒1降低了CD96在CD4+T细胞上的作用,这是一种新的免疫规避策略. 这会影响T细胞功能,并为抗艾滋病毒感染的免疫疗法提供潜在的点.

科学领域:

免疫学
病毒学
细胞生物学

背景情况:

人类免疫缺陷病毒1型 (HIV-1) 使用策略来逃避宿主免疫反应.
在CD4+ T细胞上调节血受体是病毒免疫逃避的关键机制.
CD96是一种抑制性自然杀手 (NK) 细胞受体,在人类CD4+T细胞中进行的研究有限.

研究的目的:

为了确定HIV-1感染的CD4+T细胞的表面受体调节.
研究CD96在HIV-1感染和T细胞免疫中的作用.
探索针对HIV-1的CD96的治疗潜力.

主要方法:

在HIV-1感染的原发性CD4+T细胞上对332个表面受体进行基于流细胞计的查.
病毒蛋白 (Nef和Vpu) 调节CD96的分析.
对T助手1 (T_H1) /T助手17 (T_H17) 细胞表现型,细胞因子分泌和细胞迁移的评估.
研究CD96结合对免疫反应的影响.

主要成果:

艾滋病毒-1感染下调了23个表面受体,包括CD4,MHCI,CCR7,CD62L,尤其是CD96.
艾滋病毒-1 Nef和Vpu蛋白对CD96的下调超过了其他NK相关受体的下调,并且在lentiviruses中保持不变.
CD96高 (CD96^Hi) CD4+ T细胞表现出一种促炎的T_H1/T_H17表型,IFN-γ和IL-17分泌增加,体内迁移受损.
CD96结合增强了IFN-γ的释放,并促进了T_H1/ T_H17细胞因子的分泌.

结论:

作为以前未知的免疫规避策略,HIV-1积极降低CD96在CD4+T细胞上的作用.
CD96在调节抗病毒免疫反应和维护CD4+T细胞的炎症性质方面发挥作用.
针对CD96可能是HIV-1感染的有前途的免疫治疗方法.

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