Lymphotoxin β receptor-dependent control of lipid homeostasis

James C. Lo, Yugang Wang, Alexei V. Tumanov, Michelle Bamji, Zemin Yao, Catherine A. Reardon, Godfrey S. Getz, Yang Xin Fu

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Abstract

Hyperlipidemia, one of the most important risk factors for coronary heart disease, is often associated with inflammation. We identified lymphotoxin (LT) and LIGHT, tumor necrosis factor cytokine family members that are primarily expressed on lymphocytes, as critical regulators of key enzymes that control lipid metabolism. Dysregulation of LIGHT expression on T cells resulted in hypertriglyceridemia and hypercholesterolemia. In low-density lipoprotein receptor-deficient mice, which lack the ability to control lipid levels in the blood, inhibition of LT and LIGHT signaling with a soluble lymphotoxin β receptor decoy protein attenuated the dyslipidemia. These results suggest that the immune system directly influences lipid metabolism and that LT modulating agents may represent a novel therapeutic route for the treatment of dyslipidemia.

Original languageEnglish (US)
Pages (from-to)285-288
Number of pages4
JournalScience
Volume316
Issue number5822
DOIs
StatePublished - Apr 13 2007

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Cite this

Lo, J. C., Wang, Y., Tumanov, A. V., Bamji, M., Yao, Z., Reardon, C. A., Getz, G. S., & Fu, Y. X. (2007). Lymphotoxin β receptor-dependent control of lipid homeostasis. Science, 316(5822), 285-288. https://doi.org/10.1126/science.1137221