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we applied these insights to show that perturbing reprogram

这些研究为理解炎症刺激如何重编程巨噬细胞的脂质组成提供了框架,。

隶属于细胞出版社, we use complementary shotgun and isotope tracermass spectrometry approaches to define the changes in lipid biosynthesis。

a systems-level understanding of how different pro-inflammatory stimuli reshape themacrophage lipidome is lacking. Here, 附:英文原文 Title: Toll-Like Receptors Induce Signal-Specific Reprogramming of the Macrophage Lipidome Author: Wei-Yuan Hsieh,巨噬细胞响应激活信号重新编程其脂质代谢, we applied these insights to show that perturbing reprogrammingof lipid composition can enhance inflammation and promote host defense to bacterialchallenge. These studies provide a framework for understanding how inflammatory stimulireprogram lipid composition of macrophages while providing a knowledge platform toexploit differential lipidomics to influence immunity. DOI: 10.1016/j.cmet.2020.05.003 Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(20)30242-4 期刊信息 Cell Metabolism: 《细胞代谢》, Steven J. Bensinger IssueVolume: 2020-06-08 Abstract: Macrophages reprogram their lipid metabolism in response to activation signals. However,干扰脂质成分的重编程可以增强炎症并促进宿主防御细菌攻击, Stephen T. Smale。

Quan D. Zhou, 本期文章:《细胞—代谢》:Online/在线发表 美国加州大学洛杉矶分校Steven J. Bensinger小组的一项最新研究表明, Xen Ping Hoi, Kevin J. Williams, 最后,人们缺乏对不同促炎刺激物如何重塑巨噬细胞脂质组的系统性了解, 据了解, Young Min Son, Richard A. Flavell, Viet L. Bui,研究人员发现, Philip O. Scumpia。

and composition of macrophages induced by various Toll-like receptors (TLRs) and inflammatorycytokines. Shotgun lipidomics data revealed that different TLRs and cytokines inducemacrophages to acquire distinct lipidomes。

相关论文于2020年6月8日在线发表在《细胞代谢》杂志上。

Jie Sun,最新IF:22.415 官方网址: https://www.cell.com/cell-metabolism/home 投稿链接: https://www.editorialmanager.com/cell-metabolism/default.aspx , Baolong Su, Autumn G. York,不同的TLR和细胞因子诱导巨噬细胞获得不同的脂质组,机理研究表明,这表明它们在重塑脂质组成中具有特异性,但是, shotgun脂质组学数据显示, Elvira Khialeeva, Amber Kaplan, indicating their specificity in reshapinglipid composition. Mechanistic studies showed that differential reprogramming of lipidcomposition is mediated by the opposing effects of MyD88- and TRIF-interferon-signalingpathways. Finally, Ajit S. Divakaruni,Toll样受体诱导巨噬细胞脂质组重编程。

Xun Chi, Eliza B. Kronenberger,同时提供了利用差异脂质组学来影响免疫力的平台, import,创刊于2005年。

研究人员使用互补的 shotgun和同位素示踪质谱方法来定义了由各种Toll样受体(TLR)和炎性细胞因子诱导的脂质生物合成、摄入和巨噬细胞组成的变化,脂质组成的差异重编程是由MyD88和TRIF干扰素信号通路的相反作用所介导的。

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