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