| Literature DB >> 24463443 |
Yoko Kidani, Steven J Bensinger.
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.Entities:
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Year: 2014 PMID: 24463443 PMCID: PMC3904634 DOI: 10.1172/JCI74141
Source DB: PubMed Journal: J Clin Invest ISSN: 0021-9738 Impact factor: 14.808