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增加的IFN反应驱动着艾滋病毒-1感染者的髓状细胞激活
Léo Plaçais1, Candie Joly2, Vanessa d'Urbano2
1Université Paris Saclay, AP-HP, Hôpital Bicêtre, Service de Médecine Interne et Immunologie Clinique, CEA, INSERM UMR 1184, Center for Immunology of Viral Infections and Autoimmune Diseases, Le Kremlin Bicêtre, France. leo.placais@aphp.fr.
Scientific reports
|July 2, 2025
概括
接受抗逆转录病毒治疗的艾滋病毒感染者由于持续的炎症而表现出髓状细胞活化. 作为JAK1/2抑制剂的巴里西提尼布在体外显示出逆转这种干扰素驱动的激活的潜力.
科学领域:
- 免疫学 免疫学 免疫学
- 病毒学 病毒学
- 药理学 药理学是指药理学的学科.
背景情况:
- 在慢性感染阶段开始抗逆转录病毒疗法 (ART) 的艾滋病毒感染者 (PLH) 通常会经历持续的炎症.
- 干扰素 (IFN) 和JAK-STAT信号通路与免疫细胞调节和炎症有关.
研究的目的:
- 研究IFN/JAK-STAT通路对PLH骨髓状细胞的影响.
- 评估JAK1/2抑制剂巴里西提尼布在预防PLH中IFN驱动的髓状细胞激活方面的潜力.
主要方法:
- 从16名慢性感染的,病毒学上受抑制的PLH与15名未感染个体 (UI) 的外周血液单核细胞 (PBMC) 的比较.
- PBMCs对1型IFN,2型IFN和巴里西提尼布的活体暴露.
- 骨髓细胞激活标记物的分析,包括PD-L1,CD11b和基因转录 (pd-l1,cxcl-10,ifnar1).
主要成果:
- 与UI相比,PLH髓状细胞 (单细胞,cDC2s) 活化增加,PD-L1和CD11b表达更高,pd-l1,cxcl-10和ifnar1转录增加.
- 1型和2型IFN诱导PD-L1表达,PLH髓质细胞显示出与延迟ART启动和CD4T细胞枯竭相关的增强反应.
- 巴里西替尼在体外有效地阻止了IFN驱动的PD-L1表达.
结论:
- PLH表现出与1型和2型IFN信号传递增加相关的髓状细胞激活.
- 这种激活配置和相关的IFN信号可以通过JAK1/2抑制剂,如Baricitinib在体外逆转.
- 准JAK-STAT通路可能为控制PLH炎症提供治疗潜力.
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