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结合蛋白1缺少的树突细胞通过增加Treg/Th17保护小鼠免受败血症

Xin Zhang¹, Shuang Han¹, Zhu Zeng^1,2

¹Key Laboratory of Infectious Immune and Antibody Engineering of Guizhou Province, Cellular Immunotherapy Engineering Research Center of Guizhou Province, School of Basic Medical Sciences/School of Biology and Engineering (School of Modern Industry for Health and Medicine), Guizhou Medical University, Guiyang 550025, China.

Antioxidants (Basel, Switzerland)

|April 29, 2025

概括

结合蛋白1 (SELENBP1) 在败血症中升高,并使结果恶化. 删除SELENBP1通过调节免疫细胞和减少器官损伤来改善生存率,提供潜在的败血症治疗点.

科学领域:

免疫学免疫学免疫学
分子生物学分子生物学
病理生理学病理生理学

背景情况:

结合蛋白1 (SELENBP1) 与各种疾病有关,但其在败血症引起的免疫失调和器官损伤中的作用尚不清楚.
败血症是一种危及生命的疾病,其特点是广泛的炎症和器官功能障碍.

研究的目的:

调查SELENBP1在败血症发病过程中的作用.
为了确定SELENBP1是否影响免疫细胞活动和在败血症期间的器官损伤.
探索SELENBP1作为毒症的潜在治疗点.

主要方法:

在败血症患者和败血症小鼠模型中测量了SELENBP1水平.
利用SELENBP1淘汰赛 (KO) 鼠标来评估其对败血症结局的影响.
分析了免疫细胞种群 (Treg/Th17),树突细胞 (DC) 成熟和败血性小鼠的氧化还原平衡.
研究了SELENBP1-KO成熟DCs在缓解败血症引起的肝损伤方面的治疗潜力.

主要成果:

在败血症患者和败血症小鼠肝脏中,SELENBP1水平升高.
在SELENBP1 KO小鼠中,生存时间延长,肝损伤减少,炎症减少.
缺少SELENBP1导致了更高的调控性T细胞/T辅助17细胞 (Treg/Th17) 比率,诱导了氧还原失衡,并抑制了树突细胞 (DC) 成熟,促进了耐受性DC (tolDC) 现型.
通过提高Treg/Th17比率和减少肝损伤,给SELENBP1-KO成熟的DCs改善了败血症小鼠的生存率.

结论:

通过调节免疫细胞活性,特别是树突细胞,SELENBP1在败血症的发病过程中发挥着关键作用.
向SELENBP1可能通过恢复免疫平衡和减轻器官损伤,为败血症提供一种新的治疗策略.

关键词:

树突细胞的树突细胞.氧化还原失衡氧化还原失衡结合蛋白 1 结合蛋白 1 结合蛋白已经有了血症.

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