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TLR9降低FOXO3的表达,以防止巨细胞激活综合征的过度炎症

Mengyan Wang¹, Yuning Ma¹, Jianfen Meng¹

¹Department of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.

|December 24, 2025

概括

叉头盒蛋白O3 (FOXO3) 调节成人发病斯蒂尔病与巨细胞激活综合征 (AOSD-MAS) 的炎症. 较低的FOXO3水平与疾病严重程度相关,其通过TLR9信号的抑制促进炎症.

科学领域:

免疫学免疫学免疫学
分子生物学分子生物学
类风湿病学类风湿病学

背景情况:

成人发病的斯蒂尔病 (AOSD) 涉及严重的炎症和单细胞/巨细胞过活化,可能导致巨细胞激活综合征 (MAS).
众所周知,分叉头盒蛋白O3 (FOXO3) 是一种转录因子,被干扰素降低调节,在免疫调节中发挥作用.

研究的目的:

调查FOXO3作为AOSD-MAS炎症调节者的作用.
阐明FOXO3下调背后的机制及其对疾病发病因子的影响.

主要方法:

从AOSD患者的单细胞/PBMC中分析FOXO3表达,特别是那些患有MAS的患者.
对FOXO3表达与疾病活性和炎症标志物的相关性分析.
在实验室和体内研究中,使用小鼠MAS模型和TLR9激动剂刺激的巨细胞,研究TLR9信号和AKT酸化的FOXO3调节.
在Foxo3耗尽后对巨细胞中NLRP3炎症酶激活的评估.

主要成果:

在AOSD患者的单细胞/PBMC中,FOXO3的表达显著下调,特别是那些患有MAS的患者.
较低的FOXO3水平与疾病活性和炎症标志物有负相关性.
通过转录调节和AKT介导酸化,TLR9激活诱导FOXO3下调在小鼠MAS模型和体外巨细胞培养中.
在小鼠中,Foxo3的耗尽加剧了MAS的高炎症和器官损伤,与巨细胞中NLRP3炎症酶激活的增加有关.

结论:

FOXO3是AOSD-MAS炎症的关键调节剂,其降低调节有助于疾病的发展.
TLR9信号抑制FOXO3,有助于AOSD的炎症过程.
在AOSD中,FOXO3在自我消极调节炎症方面发挥着关键作用,其通过TLR9信号抑制是关键机制.

关键词:

生物化学生物化学细胞生物学细胞生物学免疫学免疫学免疫学

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