Lymphotoxin β receptor-dependent control of lipid homeostasis Academic Article uri icon


MeSH Major

  • Lipid Metabolism
  • Liver
  • Lymphotoxin beta Receptor
  • Tumor Necrosis Factor Ligand Superfamily Member 14


  • 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 beta 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.

publication date

  • April 13, 2007



  • Academic Article



  • eng

Digital Object Identifier (DOI)

  • 10.1126/science.1137221

PubMed ID

  • 17431181

Additional Document Info

start page

  • 285

end page

  • 8


  • 316


  • 5822