转化生长因子-β,介质素-23和介质素-1β在活性多药耐药结核病期间调节TH22反应
Belén R Imperiale1, Ana Gamberale2, Noemí Yokobori3
1Institute of Experimental Medicine (IMEX)-CONICET, National Academy of Medicine, Buenos Aires City, Argentina.
Immunology
|September 16, 2023
概括
结核病患者的Th22免疫反应减弱,与较高的TGF-β水平和PD-1+ T细胞增加有关. 向TGF-β和PD-1可能会恢复结核病中的Th22功能.
科学领域:
- 免疫学 免疫学 免疫学
- 结核病研究 结核病研究
- 细胞生物学 细胞生物学
背景情况:
- 耐多药结核病 (MDR-TB) 患者表现出降低的Th22免疫反应,与较高的细菌负荷和肺损伤相关.
- 之前的一项研究表明,在MDR-TB患者中,IL-22+细胞和衰老的PD-1+T细胞之间存在逆相关性.
研究的目的:
- 调查控制系统性和Mycobacterium结核病 (Mtb) 诱导的Th22反应的调节途径,在MDR-TB,药物敏感结核病 (S-TB) 患者和健康捐赠者中进行.
- 探索IL-1β,IL-23和TGF-β等细胞因子以及PD-1/PD-L1通路在结核病进展期间Th22反应调节中的作用.
主要方法:
- 在MDR-TB,S-TB患者和健康捐赠者中对Th22反应 (IL-22+细胞) 的比较分析.
- 在血和外周血液单核细胞 (PBMC) 培养物中测量细胞因子水平 (IL-1β,IL-23,TGF-β).
- 在体外评估PD-1+T细胞比例和PD-1/PD-L1阻断对Th22反应的影响.
主要成果:
- IL-1β和IL-23促进了Mtb诱导的IL-22分泌,而TGF-β则抑制了它.
- 系统和Mtb诱导的Th22反应与TGF-β水平相反相关.
- PD-1+ T细胞数与TGF-β相关,而PD-1/PD-L1阻断增强了IL-22+细胞的扩张.
- 结核病患者的IL-23+单细胞较高;双边腔 (BCC) 与单边腔 (UCC) 患者的IL-1β+单细胞较低.
- 结核病患者的BCC显示TGF-β分泌量高于UCC患者.
结论:
- TGF-β抑制Th22反应,可能通过PD-1上调,导致结核病的免疫控制减弱.
- 显著的细胞因子 (IL-23,IL-1β,TGF-β) 与结核病的严重程度和肺腔的范围有关.
- 调节TGF-β和PD-1/PD-L1相互作用可能提供增强结核病Th22免疫力的治疗策略.
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