在毒素菌中内源性IL-27限制了早期单细胞反应及其由病态T细胞的炎症激活
Daniel L Aldridge1, Devapregasan Moodley2, Jeongho Park1,3,4
1University of Pennsylvania School of Veterinary Medicine, Philadelphia, Pennsylvania, USA.
mBio
|February 20, 2024
概括
介质素-27 (IL-27) 限制了对Toxoplasma gondii感染的免疫过度反应. 在感染期间阻断IL-27可增强免疫反应,并揭示其在调节单细胞和T细胞中的关键作用.
科学领域:
- 免疫学 免疫学 免疫学
- 寄生虫学的寄生虫学
- 分子生物学分子生物学
背景情况:
- 介质素-27 (IL-27) 对于控制T细胞介导病理在Toxoplasma gondii感染期间至关重要.
- 内源IL-27在调节对T. gondii的免疫反应中的精确时间和作用尚未完全理解.
研究的目的:
- 调查内源性IL-27对野生类型小鼠对T. gondii的免疫反应的影响.
- 为了确定感染的特定阶段和T. gondii感染期间由IL-27调节的细胞类型.
主要方法:
- 在受感染的野生类型小鼠中,单细胞产生IL-27p28的分析.
- 在感染的急性和慢性阶段给予抗IL-27p28抗体.
- 通过细胞性,细胞因子生产和转录概况评估免疫细胞激活,效应T细胞反应和病理学.
主要成果:
- IL-27p28是由炎症单细胞早期产生的,并在整个感染过程中持续存在.
- 在急性感染期间阻断IL-27增强了先天性免疫激活和效应T细胞反应,导致病理.
- 在慢性感染期间阻断IL-27增强了T细胞反应而不会引起系统性病理,这表明IL-27的抑制作用.
结论:
- 内源IL-27在T. gondii感染期间调节先天性和适应性免疫反应方面发挥着关键的抑制作用.
- 在活跃的感染阶段,IL-27是必不可少的,特别是在寄生虫复制部位调节单细胞和T细胞的反应.
- 单细胞是由IL-27调节的关键细胞类型,有助于了解寄生虫感染中IL-27的调节网络.
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