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通过调节TRADD,降低BIRC2的调节阻碍了类风湿性关节炎的进展
Yanting Rao1, Shengjing Xu1, Ting Lu1
1Department of Rheumatology and Immunology, The Affiliated Jiangning Hospital of Nanjing Medical University, Nanjing, China.
Immunity, inflammation and disease
|October 31, 2023
概括
减少巴库洛病毒IAP重复含有2 (BIRC2) 减少了风湿性关节炎 (RA) 模型中的死亡,氧化应激和炎症. 这种效应与TRADD的调节有关,这表明RA的新治疗标.
科学领域:
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 类风湿性关节炎 (RA) 是一种慢性自身免疫性疾病,其特征是炎症.
- 细菌病毒IAP重复含有2 (BIRC2) 和瘤亡因子受体1-关联死亡域蛋白 (TRADD) 在RA中被上调.
- 在RA病变发生过程中,BIRC2和TRADD的确切作用尚不完全理解.
研究的目的:
- 调查BIRC2和TRADD在类风湿性关节炎进展过程中的特定调节功能.
- 为了探索BIRC2和TRADD之间的相互作用在体外RA细胞模型中.
主要方法:
- 通过使用脂多糖 (LPS) 刺激的C28/I2细胞建立了体外RA细胞模型.
- 使用定量实时聚合酶连锁反应和西布洛特来评估BIRC2和TRADD表达.
- 测量了细胞活力,亡,氧化应激标志物和促炎细胞因子.
主要成果:
- 在LPS诱导的C28/I2细胞中,BIRC2和TRADD的表达很高.
- BIRC2倒置显著抑制了LPS诱导的细胞活力丧失,亡,氧化应激和炎症.
- 发现BIRC2与TRADD表达相互作用并积极调节;TRADD过度表达部分逆转了BIRC2敲击的保护作用.
结论:
- 在LPS介导的RA模型中,BIRC2敲击减轻了亡,氧化应激和炎症.
- BIRC2的保护作用可能通过其对TRADD的调节来调节.
- 针对BIRC2及其与TRADD的相互作用,为类风湿性关节炎提供了潜在的治疗策略.
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