芝加哥大学医疗中心的研究人员在小鼠研究中，发现了免疫系统和高血浆脂质(血液中的胆固醇和三酸甘油酯)含量之间的关连性。
这项发表于2007 年4月13 日Science中的研究结果，有助于研发出新方法，降低升高的脂质含量。这项研究设计出的蛋白质，将可以使小鼠免于胆固醇和三酸甘油酯含量过高，这二项都是冠状动脉心脏病的重要风险因素。
这项研究除了证实免疫系统和增加的脂质间的关连性，这项研究也开启了新的路径，有助于研究增加的血液脂质与慢性发炎之间的关连性。
研究人员利用经过设计和未经过设计的小鼠，观察T 细胞的角色。他们发现T细胞上的LIGHT及lymphotoxin (LT)表现量改变，对于胆固醇和三酸甘油酯含量有很大的影响。
这项研究显示，肝脏的T细胞在脂肪的代谢中扮演相当重要的角色。例如狼疮、类风湿性关节炎和发炎性肠道症候群，都有较高的心血管疾病发生率，经常与增加的血液脂质含量有关。
(资料来源 : biocompare)
英文原文链接：http://news.biocompare.com/newsstory.asp?id=178255
原始出处:
Science 13 April 2007:
Vol. 316. no. 5822, pp. 285 - 288
DOI: 10.1126/science.1137221
Reports
Lymphotoxin ß Receptor–Dependent Control of Lipid Homeostasis
James C. Lo,1* Yugang Wang,2* Alexei V. Tumanov,2* Michelle Bamji,3 Zemin Yao,3 Catherine A. Reardon,2 Godfrey S. Getz,2 Yang-Xin Fu1,2
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 ß 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.
1 Committee on Immunology, University of Chicago, Chicago, IL 60637, USA.
2 Department of Pathology, University of Chicago, Chicago, IL 60637, USA.
3 Department of Biochemistry, Microbiology and Immunology, University of Ottawa Heart Institute, Ottawa, Ontario K1H 8M5, Canada.
* These authors contributed equally to this work.
To whom correspondence should be addressed. E-mail: yfu@uchicago.edu (Y.-X.F.); getz@bsd.uchicago.edu (G.S.G.)
