由肠道微生物群真核生物制成的托芬代谢物诱导亲炎性T细胞
Lukasz Wojciech1,2, Chin Wen Png1,2,3, Eileen Y Koh2,4
1Immunology Translational Research Programme, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
The EMBO journal
|September 25, 2023
概括
前列腺母细胞体ST7感染减少调节性T细胞 (Treg) 和扩大炎症性T细胞 (Th17) 在肠道. 这种不平衡是由代谢物英多尔-3-乙甲 (I3AA) 驱动的,影响宿主免疫反应.
科学领域:
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
- 胃肠病学 胃肠病学
背景情况:
- 肠道微生物群影响宿主生理学,CD4+ T细胞平衡对免疫平衡至关重要.
- 失生症和改变的T细胞种群与性结肠炎等炎症性肠道疾病有关.
研究的目的:
- 调查原体细胞母细胞ST7在调节肠道CD4+T细胞反应中的作用.
- 为了确定细胞囊胚性ST7影响免疫细胞群和宿主炎症的机制.
主要方法:
- 利用小鼠模型感染了Blastocystis ST7以研究性结肠炎类变化.
- 分析了CD4+T细胞子集 (Treg和Th17) 和它们的功能.
- 研究了三的代谢物英多尔-3-乙甲 (I3AA) 在调解免疫变化的作用.
主要成果:
- 胚囊ST7感染导致大肠中Treg细胞减少,Th17细胞增加.
- 蛋白质原体衍生代谢物I3AA被确定为这些CD4+T细胞变化的关键媒介.
- I3AA通过改变TGFβ传感和增强T细胞受体 (TCR) 信号传递,损害了Treg发育.
结论:
- 细胞囊体ST7感染通过代谢物I3AA.破坏了肠道免疫平衡.
- I3AA调节CD4+T细胞命运,导致炎症.
- 这突显了一种涉及前列腺体代谢物在适应性免疫和肠道炎症疾病中的新奇机制.
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