MafB通过维持巨细胞中的p62表达来调节NLRP3炎症酶激活
Huachun Cui1, Sami Banerjee1, Na Xie1
1Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, 35294, USA.
Communications biology
|October 16, 2023
概括
MafB蛋白质负面调节NLRP3炎症体,这是一个关键的免疫通路. 提高MafB可以治疗因过度NLRP3炎症酶激活引起的炎症性疾病.
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:
- NLRP3炎症酶激活是一个关键的两步过程,涉及原始化和激活.
- 虽然已知激活机制,但调节途径尚不清楚.
- MafB蛋白在炎症酶调节中的作用尚不清楚.
研究的目的:
- 研究MafB在调节炎性酶激活中的作用.
- 阐明MafB影响NLRP3炎症酶活性的分子机制.
主要方法:
- 使用的巨细胞与MafB淘汰/淘汰和药理学诱导.
- 评估了炎症酶激活 (NLRP3,NLRC4,AIM2,NLRP1) 和细胞因子的产生 (IL-1β).
- 研究了MafB对p62的表达,自/线粒体,线粒体损伤和ROS的生体和体外产生的影响.
主要成果:
- LPS和Pseudomonas aeruginosa降低了巨细胞中的MafB水平.
- MafB 缺乏增强了 NLRP3 炎症酶激活,而 MafB 诱导则抑制了它.
- MafB维持p62的表达,抑制线粒体损伤,并减少ROS的产生.
结论:
- MafB作为NLRP3炎症酶的关键负调节剂.
- 马夫B缺乏会加剧IL-1β的产生,并影响细菌的清除.
- 针对MafB可以为NLRP3驱动的炎症条件提供治疗策略.
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