在肺结核中,ILC2s通过IL-33/ST2通路诱导Treg,但不诱导Th2型免疫
Qifeng Li1, Quan Wang2, Zhenhua Xu1
1Xinjiang Institute of Pediatrics, Children's Hospital of Xinjiang Uygur Autonomous Region Xinjiang Hospital of Beijing Children's Hospital, Urumqi, Xinjiang 830054, China.
Journal of infection in developing countries
|July 11, 2024
概括
介素-33 (IL-33) 可能在肺结核 (PTB) 中促进2型先天性淋巴细胞 (ILC2s) 和调节性T细胞 (Treg) 细胞因子的产生. 这表明IL-33和ILC2在PTB免疫反应中起作用.
科学领域:
- 免疫学 免疫学 免疫学
- 传染性疾病 传染性疾病
- 细胞生物学 细胞生物学
背景情况:
- 肺结核 (PTB) 是一个重要的全球卫生挑战.
- 2型先天性淋巴细胞 (ILC2s) 和IL-33在PTB发病过程中的作用仍然不完全理解.
研究的目的:
- 研究ILC2s和IL-33在对PTB的免疫反应中的功能.
- 确定PTB患者IL-33,ILC2s和T细胞子集之间的关系.
主要方法:
- 在PTB患者和健康对照者中测量了IL-33,sST2和各种细胞因子 (IL-4,IL-5,IL-6,IL-10,IL-13,TGF-β) 的血水平.
- 使用流细胞计量量化ILC2s,Th2细胞和Treg细胞.
- 在体外实验中,ILC2s与外周血液单核细胞共同培养,并用IL-33.3刺激.
主要成果:
- 与健康对照组相比,PTB患者的IL-33,sST2,TGF-β,IL-10和IL-6的血含量显著增加.
- 在PTB患者中观察到ILC2s关键转录因子的比例和mRNA水平增加.
- 实验室IL-33刺激导致Treg细胞比例增加和IL-10的产生,这被反ST2治疗取消.
结论:
- IL-33可能促进ILC2的扩散和Treg相关细胞因子的产生,从而促进PTB的免疫反应.
- 这些发现表明,一种潜在的机制涉及IL-33和ILC2s在PTB期间调节T调节细胞反应.
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