芝加哥大學醫(yī)療中心的研究人員在小鼠研究中,，發(fā)現(xiàn)了免疫系統(tǒng)和高血漿脂質(zhì)(血液中的膽固醇和三酸甘油酯)含量之間的關連性,。
這項發(fā)表于2007 年4月13 日Science中的研究結(jié)果,，有助于研發(fā)出新方法,，降低升高的脂質(zhì)含量,。這項研究設計出的蛋白質(zhì),，將可以使小鼠免于膽固醇和三酸甘油酯含量過高,，這二項都是冠狀動脈心臟病的重要風險因素。
這項研究除了證實免疫系統(tǒng)和增加的脂質(zhì)間的關連性,，這項研究也開啟了新的路徑,，有助于研究增加的血液脂質(zhì)與慢性發(fā)炎之間的關連性。
研究人員利用經(jīng)過設計和未經(jīng)過設計的小鼠,，觀察T 細胞的角色,。他們發(fā)現(xiàn)T細胞上的LIGHT及l(fā)ymphotoxin (LT)表現(xiàn)量改變，對于膽固醇和三酸甘油酯含量有很大的影響,。
這項研究顯示,，肝臟的T細胞在脂肪的代謝中扮演相當重要的角色。例如狼瘡,、類風濕性關節(jié)炎和發(fā)炎性腸道癥候群,，都有較高的心血管疾病發(fā)生率，經(jīng)常與增加的血液脂質(zhì)含量有關,。
(資料來源 : biocompare)
英文原文鏈接：http://news.biocompare.com/newsstory.asp?id=178255
原始出處:
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: [email protected] (Y.-X.F.); [email protected] (G.S.G.)
