CD5L/AIM 调节脂质生物合成并抑制Th17细胞的致病性
Chao Wang1, Nir Yosef2, Jellert Gaublomme3
1Evergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
Cell
|November 27, 2015
概括
CD5L/ AIM蛋白调节T助手17 (Th17) 细胞的致病性,防止自身免疫. 通过改变脂质代谢,CD5L的损失将非致病的Th17细胞转化为致病细胞.
科学领域:
- 免疫学
- 细胞生物学
- 代谢途径
背景情况:
- 辅助T细胞17 (Th17) 对于免疫非常重要,但也可能导致自身免疫性疾病.
- 控制致病与非致病的Th17细胞状态的机制尚未完全理解.
研究的目的:
- 识别分辨致病性和非致病性Th17细胞子集的关键调节者.
- 阐明CD5L/AIM在调节Th17细胞致病性的功能作用.
主要方法:
- 单细胞RNA测序 (scRNA-seq) 来识别差异性基因表达.
- 功能性测试以评估CD5L对Th17细胞的体内致病性的影响.
- 细胞内脂质代谢和转录因子活性的分析.
主要成果:
- CD5L/ AIM被确定为非致病性Th17细胞的标志物,在致病性亚组中不存在.
- CD5L缺乏将非致病的Th17细胞转化为致病的自身免疫表型.
- CD5L通过调节细胞内脂质组来调节Th17的致病性,影响胆固醇生物合成和Rorγt活性.
结论:
- CD5L/AIM充当控制Th17细胞致病性的关键开关.
- 脂质代谢是平衡免疫反应和由Th17细胞介导的自身免疫疾病的关键决定因素.
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