在病毒感染后,微质体不需要CD11c来传递神经保护
James A Carroll1, James F Striebel1, Chase Baune1
1Laboratory of Neurological Infections and Immunity, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, United States of America.
PloS one
|November 1, 2023
概括
在小鼠中删除CD11c并没有改变子疾病的进展或神经病理. 微细胞CD11c信号传递对神经保护并不重要,但子感染会激活中枢神经系统中独特的细胞化途径.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 蛋白质错折叠疾病 蛋白质错折叠疾病
背景情况:
- 子疾病涉及错误折叠的宿主蛋白质,导致神经炎症和神经退行.
- 在子感染期间,微细胞对中枢神经系统 (CNS) 的神经保护至关重要,延长了生存期.
- 微质提供神经保护的具体机制尚不清楚,尽管假设CD11c/CD18整合蛋白信号传递是重要的.
研究的目的:
- 调查CD11c/CD18整合蛋白信号传递在病期间微质功能中的作用.
- 确定微质细胞的CD11c表达是否对中枢神经系统的神经保护至关重要.
- 为了确定参与微质对子感染的反应的分子通路.
主要方法:
- 具有RML子菌株的CD11c淘汰 (CD11c-/-) 小鼠的脑内挑战.
- 对CD11c-/-小鼠与野生型C57BL/6小鼠进行疾病标志物 (结晶症,微结晶症,子积累,存活率) 的比较.
- 向定量逆转录PCR (qRT-PCR) 阵列用于分析因感染而发生的基因表达变化.
主要成果:
- CD11c (Itgax) 和CD18 (Itgb2) 表达在中枢神经系统中随着子感染的进展而增加.
- 与对照组相比,缺少CD11c并没有影响滑症,神经病理学,质沉积或疾病进展.
- 缺乏CD11c的小鼠和对照小鼠在疾病进展过程中表现出炎症和细胞结合相关基因表达的增加.
结论:
- CD11c信号传递与质病原发生过程中微质的神经保护作用无关.
- 删除CD11c不会影响小鼠的普里昂病的整体过程.
- 子感染激活了中枢神经系统中独特的细胞化途径,独立于CD11c信号传递.
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