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线粒体ROS通过气皮D介导的亡促进了感染的易感性

Chi G Weindel¹, Eduardo L Martinez¹, Xiao Zhao²

¹Department of Microbial Pathogenesis and Immunology, Texas A&M Health, College of Medicine, Bryan, TX 77807, USA.

|July 30, 2022

概括

突变的LRRK2破坏了线粒体功能,导致巨细胞转向死亡. 这会导致超炎症和严重的病理反应.

科学领域:

免疫学
细胞生物学
线粒体生物学

背景情况:

线粒体基因的突变与炎症和感染易感性有关.
连接线粒体功能障碍与免疫反应的机制尚未完全理解.

研究的目的:

调查Lrrk2 G2019S突变如何影响巨细胞的线粒体平衡和细胞死亡途径.
在Lrrk2突变的背景下阐明气体皮质D (GSDMD) 在调解细胞死亡和免疫反应中的作用.

主要方法:

使用表达Lrrk2 G2019S功能增益等位体的巨细胞.
分析了炎症酶激活,线粒体反应性氧物种 (mtROS) 生产和细胞死亡途径 (亡).
感染了Mycobacterium结核病的Lrrk2 G2019S小鼠,以评估体内免疫病理.

主要成果:

这种Lrrk2 G2019S突变会扰乱线粒体平衡,并重编程细胞死亡.
在Lrrk2 G2019S巨中升高的mtROS将GSDMD导向线粒体膜,促进亡.
在Lrrk2 G2019S小鼠感染 Mycobacterium tuberculosis后,由于死亡的增加,它们呈现出高炎症和严重的免疫病态.

结论:

线粒体功能障碍可以通过切换细胞死亡方式来决定免疫结果.
GSDMD是多种细胞死亡途径的关键执行者,包括亡.
向GSDMD依赖性亡可能会减轻LRRK2突变相关的免疫病理.

关键词:

这种植物是Drosophila melanogaster.其他类型结核菌帕金森病在RIPK 免疫新陈代谢炎症组发生炎症天生的免疫力热症

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