IL-10 抑制了脂代谢,以限制炎症
Autumn G York1,2,3, Mathias H Skadow4, Joonseok Oh5,6
1Department of Immunobiology, Yale University, New Haven, CT, USA. AGYork@UW.edu.
Nature
|February 21, 2024
概括
由于长链胺的增加,介质素-10 (IL-10) 缺乏会引起炎症. 恢复脂肪酸合成解决了这一问题,突出了炎症性疾病的代谢纠正.
科学领域:
- 免疫学
- 代谢途径
- 细胞生物学
背景情况:
- 互白素-10 (IL-10) 是一种重要的抗炎细胞因子.
- 失去IL-10信号会导致严重的炎症状况,如炎症性肠病.
- 通过IL-10抑制炎症的确切机制尚未完全理解.
研究的目的:
- 阐明IL-10抗炎功能的分子机制.
- 研究非常长链 (VLC) 陶在IL-10缺乏导致的炎症中的作用.
- 探索针对代谢途径的潜在治疗策略.
主要方法:
- 在IL-10缺陷模型中研究基因表达.
- 利用胺合成酶2 (Cers2) 的遗传删除来抑制VLC胺的产生.
- 操作的单不和脂肪酸合成途径.
- 评估了转录因子REL的活性.
主要成果:
- 在IL-10缺乏中,炎症基因表达的增加与和VLC胺的增加有关.
- 在缺乏IL-10的模型中,基因删除Cers2或恢复脂肪酸合成减少了炎症.
- 由VLC胺介导的炎症取决于持续的REL活动.
- IL-10信号调节影响VLC胺代谢的脂肪酸脱程序.
结论:
- 通过调节脂肪酸代谢和防止VLC胺的积累,IL-10信号控制炎症.
- 异常的VLC胺代谢和REL激活有助于IL-10缺乏的病理.
- 对IL-10相关的炎症性疾病进行代谢纠正是潜在的治疗方法.
相关概念视频
T Cell Types and Functions
1.0K
When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
1.0K
Inflammatory Response
2.0K
An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
2.0K
The JAK-STAT Signaling Pathway
8.9K
Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...
8.9K
IP3/DAG Signaling Pathway
12.1K
Membrane lipids such as phosphatidylinositol (PI) are precursors for several membrane-bound and soluble second messengers. Specific kinases phosphorylate PI and produce phosphorylated inositol phospholipids. One such inositol phospholipids are the phosphatidylinositol-4,5 bisphosphate [PI(4,5)P2], present in the inner half of the lipid bilayer. Upon ligand binding, GPCR stimulates Gq proteins to turn on phospholipase Cꞵ. Activated phospholipase Cꞵ cleaves PI(4,5)P2 and...
12.1K
TGF - β Signaling Pathway
7.4K
The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
7.4K
Inflammation
53.4K
Overview
53.4K


