通过TRIM24介导的STAT6乙化抑制了Th2诱导的过敏性鼻炎
Liyan Yue1, Qiaojing Jia1, Jinhui Dong2
1ENT Department 1, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Allergy, asthma & immunology research
|October 12, 2023
概括
含有三部分基因的24 (TRIM24) 通过调节信号传感器和转录6 (STAT6) 乙化激活剂来抑制过敏性鼻炎 (AR). 在AR患者中,较低的TRIM24表达与疾病严重程度的增加相关.
科学领域:
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
- 过敏研究 研究过敏
背景情况:
- 过敏性鼻炎 (AR) 是一种T助手2型 (Th2) 介导的炎症性疾病.
- E3结合酶TRIM24影响STAT6的乙化,影响其活性.
- TRIM24在AR病变发生中的特定作用需要进一步阐明.
研究的目的:
- 在过敏性鼻炎的背景下研究TRIM24的功能.
- 探索TRIM24影响AR中的Th2介导炎症的分子机制.
主要方法:
- 从AR患者的外周血液单核细胞 (PBMC) 和CD4+T细胞中测量TRIM24表达.
- 产生的TRIM24条件淘汰赛小鼠,缺乏CD4+T细胞.
- 在野生类型和淘汰赛小鼠中评估了AR症状,IL-4水平,CD4+T细胞增殖,激活,极化和STAT6活性.
主要成果:
- 在AR患者的PBMC和CD4+T细胞中,TRIM24表达被下调.
- 缺乏TRIM24的小鼠表现出加剧的AR症状和增加的IL-4产量.
- 由于STAT6乙化减少,TRIM24缺乏导致Th2极化增强和STAT6活性增加.
结论:
- TRIM24在Th2介导的过敏性鼻炎中起抑制作用.
- TRIM24通过调节STAT6乙化和活性来调节AR.
- TRIM24的功能与其N端RIGN域和STAT6 Lys383乙化位点有关.
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