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持续的T细胞不响应与慢性内脏莱什曼病相关,在艾滋病毒共感染患者中

Nicky de Vrij^1,2, Julia Pollmann³, Antonio M Rezende⁴

¹Clinical Immunology Unit, Department of Clinical Sciences, Institute of Tropical Medicine, 2000, Antwerp, Belgium.

Communications biology

|May 3, 2024

概括

慢性艾滋病毒共同感染的内脏莱什曼病 (VL-HIV) 患者由于高TIGIT和PD-1水平而表现出T细胞功能受损. 这表明这些标志物可以指导复发性VL-HIV疾病的风险分层和免疫治疗.

科学领域:

免疫学免疫学免疫学
传染性疾病传染性疾病
艾滋病毒/艾滋病研究研究

背景情况:

艾滋病毒共感染患者 (VL-HIV) 的内脏莱什曼病 (VL) 通常导致慢性疾病和频繁复发.
驱动VL-HIV慢性病程和复发的免疫因素尚不清楚.

研究的目的:

研究埃塞俄比亚患者的慢性疾病和复发的免疫学决定因素,艾滋病毒共感染和内脏莱什曼病.
确定潜在的风险分层生物标志物和VL-HIV的治疗目标.

主要方法:

在埃塞俄比亚的一组艾滋病毒感染个体中,循环细胞免疫的纵向分析,包括那些患有VL的人.
使用T细胞受体谱,单T细胞转录组学,以及免疫检查点标记物 (TIGIT,PD-1) 和细胞因子生产 (IFN-γ) 的评估来分析T细胞功能.

主要成果:

慢性VL-HIV患者在CD8+和CD8-T细胞上表现出持续升高的TIGIT和PD-1水平.
观察到IFN-γ产生TIGIT-T细胞的频率降低,表明T细胞功能受损.
单细胞分析揭示了CD4+T细胞无能性,其特征是抑制T细胞激活和淋巴增殖反应.

结论:

在T细胞上PD-1和TIGIT的高和持续表达与VL-HIV的慢性和复发有关.
这些免疫检查点分子可以作为分层患者风险的关键生物标志物.
针对PD-1和TIGIT的辅助免疫疗法是治疗慢性VL-HIV并预防疾病复发的有希望的策略.

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