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本文引用的文献

1
Normalizing glycosphingolipids restores function in CD4+ T cells from lupus patients.糖脂正常化恢复狼疮患者 CD4+T 细胞的功能。
J Clin Invest. 2014 Feb;124(2):712-24. doi: 10.1172/JCI69571. Epub 2014 Jan 27.
2
LXRs regulate ER stress and inflammation through dynamic modulation of membrane phospholipid composition.LXRs 通过动态调节膜磷脂组成来调节 ER 应激和炎症。
Cell Metab. 2013 Nov 5;18(5):685-97. doi: 10.1016/j.cmet.2013.10.002.
3
LXR-mediated inhibition of CD4+ T helper cells.LXR 介导的 CD4+ T 辅助细胞抑制。
PLoS One. 2012;7(9):e46615. doi: 10.1371/journal.pone.0046615. Epub 2012 Sep 28.
4
Transcriptional integration of metabolism by the nuclear sterol-activated receptors LXR and FXR.核甾醇激活受体 LXR 和 FXR 对代谢的转录整合。
Nat Rev Mol Cell Biol. 2012 Mar 14;13(4):213-24. doi: 10.1038/nrm3312.
5
Coordinate regulation of neutrophil homeostasis by liver X receptors in mice.肝 X 受体在小鼠中性粒细胞稳态中的协调调控作用。
J Clin Invest. 2012 Jan;122(1):337-47. doi: 10.1172/JCI58393. Epub 2011 Dec 12.
6
Systemic lupus erythematosus.系统性红斑狼疮
N Engl J Med. 2011 Dec 1;365(22):2110-21. doi: 10.1056/NEJMra1100359.
7
Apoptotic cells promote their own clearance and immune tolerance through activation of the nuclear receptor LXR.凋亡细胞通过激活核受体LXR促进自身清除和免疫耐受。
Immunity. 2009 Aug 21;31(2):245-58. doi: 10.1016/j.immuni.2009.06.018. Epub 2009 Jul 30.
8
LXR regulates cholesterol uptake through Idol-dependent ubiquitination of the LDL receptor.肝脏X受体通过依赖Idol的低密度脂蛋白受体泛素化作用来调节胆固醇摄取。
Science. 2009 Jul 3;325(5936):100-4. doi: 10.1126/science.1168974. Epub 2009 Jun 11.
9
Differential expression and molecular associations of Syk in systemic lupus erythematosus T cells.系统性红斑狼疮T细胞中Syk的差异表达及分子关联
J Immunol. 2008 Dec 1;181(11):8145-52. doi: 10.4049/jimmunol.181.11.8145.
10
Integration of metabolism and inflammation by lipid-activated nuclear receptors.脂质激活核受体介导的代谢与炎症整合
Nature. 2008 Jul 24;454(7203):470-7. doi: 10.1038/nature07202.

脂质主宰:重塑脂质代谢可恢复系统性红斑狼疮患者 T 细胞功能。

Lipids rule: resetting lipid metabolism restores T cell function in systemic lupus erythematosus.

出版信息

J Clin Invest. 2014 Feb;124(2):482-5. doi: 10.1172/JCI74141. Epub 2014 Jan 27.

DOI:10.1172/JCI74141
PMID:24463443
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3904634/
Abstract

Systemic lupus erythematosus (SLE) is a devastating autoimmune disease characterized by chronic inflammation and systemic destruction of host organs or tissue. A key feature of SLE is T cell dysfunction characterized by hyperresponsive antigen receptor signaling. In this issue of the JCI, McDonald and colleagues provide evidence that homeostasis of a subset of lipids, the glycosphingolipids (GSLs), is severely perturbed in the membranes of T cells from SLE patients. Furthermore, normalization of GSLs restored TCR signaling and ameliorated T cell dysfunction. These data suggest that targeting host metabolism may be an effective means of reinforcing self-tolerance and attenuating autoimmunity.

摘要

系统性红斑狼疮(SLE)是一种破坏性的自身免疫性疾病,其特征是慢性炎症和宿主器官或组织的系统性破坏。SLE 的一个关键特征是 T 细胞功能障碍,其特征是抗原受体信号的超反应性。在本期 JCI 中,McDonald 及其同事提供了证据,表明糖脂(GSL)这一组分的脂质稳态在 SLE 患者的 T 细胞的膜中受到严重破坏。此外,GSL 的正常化恢复了 TCR 信号传导,并改善了 T 细胞功能障碍。这些数据表明,靶向宿主代谢可能是增强自身耐受和减弱自身免疫的有效手段。