通过CARD9剥离诱导的线粒体介导的铁灭可以防止MDSCs依赖的抗真菌免疫
Zhiyong Zhang1,2,3, Pengfei Li2,3, Ying Chen2,3
1Department of Endodontic, Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Research Institute of Stomatology, Nanjing University, Nanjing, 210008, China.
Cell communication and signaling : CCS
|April 2, 2024
概括
卡斯帕斯招募域含有蛋白9 (CARD9) 除增强了骨髓衍生抑制细胞 (MDSC) 中的铁亡,损害了抗真菌免疫力. 向这种铁亡提供了一种新的治疗策略,用于在扩散性 кандидоз期间的损伤.
科学领域:
- 免疫学 免疫学 免疫学
- 菌类学 菌类学是指菌类学.
- 脏病理学 脏病理学
背景情况:
- 含有卡斯帕斯招募域的蛋白9 (CARD9) 对于针对散播性 кандидоз的髓状细胞介导的抗真菌免疫至关重要.
- 遗传性CARD9缺陷导致致命的传播性角膜炎,但潜在的髓状细胞类型和分子机制尚不清楚.
研究的目的:
- 阐明CARD9在预防扩散性候群病中的作用,并确定CARD9切除诱导的损伤的分子机制.
- 调查CARD9缺陷对髓质衍生抑制细胞 (MDSC) 和它们对铁亡的敏感性的影响.
主要方法:
- 在体内和体外研究评估了CARD9除在扩散性角膜病的作用.
- 通过RNA测序分析,确定了将CARD9除与急性损伤联系起来的分子机制.
- 定量实时PCR和西斑测量了线粒体和铁化相关蛋白质表达.
主要成果:
- 卡尔迪9切除减少了脏MDSCs和溶解物载体家族7成员11 (SLC7A11) 的表达,增加了在Candida tropicalis感染期间对急性损伤和铁亡的易感性.
- 由于减少SLC7A11.7A的线粒体氧化酸化 (OXPHOS) 的增加,CARD9缺乏的MDSCs表现出铁亡.
- Syk-PKCδ-CARD9-FosB信号轴调节MDSC中的SLC7A11表达,其中FosB与SLC7A11促进子结合.
结论:
- CARD9 除促进了MDSCs中线粒体介导的铁亡,对抗真菌免疫产生负面影响.
- 在MDSC中由线粒体介导的铁亡是一种新的机制,它是分散型 кандидоз中CARD9除加剧的急性损伤的基础.
- 向线粒体介导的铁亡是一种潜在的治疗策略,用于扩散型 кандидоз相关的急性损伤.
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