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在抑制性ART的HIV-1感染期间,持续的I型干扰素信号会损害先天性淋巴细胞

Runpeng Han¹, Haisheng Yu^2,3, Guangming Li^2,4

¹State Key Laboratory of Virology and Biosafety, Department of Infectious Diseases, Medical Research Institute, Frontier Science Center for Immunology and Metabolism, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan 430071, China.

|August 28, 2025

概括

在HIV-1感染中,持续的I型干扰素 (IFN- I) 信号破坏自然杀手细胞 (NK) 和3组先天性淋巴细胞 (ILC3). 阻断IFN- I信号恢复免疫功能,这对于控制HIV-1和粘膜免疫是至关重要的.

科学领域:

免疫学
病毒学
传染性疾病

背景情况:

已知持续的I型干扰素 (IFN- I) 信号会损害抗HIV- 1T细胞免疫力,并导致病毒储存库的持续性.
在HIV-1感染期间,慢性IFN- I对先天性淋巴细胞 (ILC) 的影响尚不清楚.

研究的目的:

在慢性HIV-1感染的背景下,研究持续的IFN-I信号对自然杀手细胞 (NK) 和3组先天性淋巴细胞 (ILC3) 的影响.
探索阻断IFN-I信号的潜力,以恢复先天性淋巴细胞功能并增强抗病毒和粘膜免疫力.

主要方法:

综合单细胞RNA测序用于分析HIV-1感染的人类化小鼠的免疫细胞群.
功能验证与联合抗逆转录病毒疗法 (cART) 和IFN- I信号阻断一起进行.
这项研究研究了IFN- I- CD9轴在NK细胞功能障碍中的作用.

主要成果:

在慢性HIV-1感染期间,IFN- I信号诱导NK细胞和ILC3细胞的功能障碍.
IFN-I-CD9轴促进了类似NK细胞的型,导致细胞毒性活性受损.
IFNAR封锁有效地挽救了ILC3的功能,恢复了对抗菌防御和粘膜屏障完整性至关重要的IL-17/IL-22的产生.

结论:

在HIV-1感染中,持续的IFN-I信号驱动多个先天性淋巴细胞区的免疫抑制.
针对IFN- I途径的制是一种有前途的策略,可以在HIV-1治疗中增强抗病毒和粘膜免疫力.
恢复ILC3功能对于保持粘膜屏障完整性和对病原体的防御至关重要.

关键词:

人类免疫缺陷病毒人性化小鼠免疫病原发生原生淋巴细胞一种类型的干扰素

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