在克罗恩病中,AIEC依赖的致病性Th17细胞转基因分化被rfaP和ybaT删除抑制
G Leccese1, M Chiara1, I Dusetti1
1Department of Biosciences, Università degli Studi di Milano, Milan, Italy.
Gut microbes
|July 29, 2024
概括
粘附性侵入性大肠杆菌 (AIEC) 通过促进致病性Th17细胞驱动克罗恩病. 确定了新的目标ybaT和rfaP,以阻止这种炎症途径.
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:
- 粘附性侵入性大肠杆菌 (AIEC) 和致病性Th17 (pTh17) 细胞与克罗恩氏病 (CD) 的致病性有关.
- 在CD中,AIEC驱动的pTh17细胞分化的精确分子机制尚不清楚.
研究的目的:
- 确定AIEC致病因子,负责诱导CD患者的IL-23生产和pTh17细胞生成.
- 研究树突细胞 (DC) 和特定的AIEC基因在这个过程中的作用.
主要方法:
- 对AIEC大型转子子子突变库的选,以确定关键的毒性基因.
- 同培养AIEC感染的人类树突细胞 (DCs) 与来自健康捐赠者和CD患者的常规Th17 (cTh17) 细胞.
- 评估pTh17细胞转分化和IL-23的产生.
主要成果:
- AIEC诱导IL-23高分泌和cTh17到pTh17细胞转分化,具体通过CD患者衍生的DCs.
- 需要持续的IL-23中和来减少AIEC依赖的pTh17细胞分化.
- 删除AIEC基因*ybaT*或*rfaP*显著降低IL-23高分泌和pTh17细胞生成.
结论:
- 细菌基因 *ybaT* 和 *rfaP* 对于 AIEC 中介的 IL-23 生产和 CD 中的致病性 Th17 细胞分化至关重要.
- *ybaT*和*rfaP*是预防克罗恩病慢性肠道炎症的有希望的治疗点.
关键词:
AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC AIEC克罗恩氏病是什么 克罗恩氏病是什么它们有IL-23和IL-23.致病的 Th17 细胞.更多相关视频
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