Scavenger receptor class B type I and immune dysfunctions

被引:24
|
作者
Zheng, Zhong [1 ,2 ]
Ai, Junting [1 ,2 ]
Li, Xiang-An [1 ,2 ,3 ]
机构
[1] Univ Kentucky, Coll Med, Dept Pediat, Lexington, KY USA
[2] Univ Kentucky, Coll Med, Grad Ctr Nutr Sci, Lexington, KY USA
[3] Univ Kentucky, Coll Med, Saha Cardiovasc Res Ctr, Lexington, KY USA
关键词
atherosclerosis; dysfunctions; HDL; immunity; inflammation; sepsis; SR-BI; HIGH-DENSITY-LIPOPROTEIN; HEPATITIS-C VIRUS; NITRIC-OXIDE SYNTHASE; ATHEROSCLEROTIC LESION DEVELOPMENT; IMPROVES SEPSIS SURVIVAL; MARROW-DERIVED CELLS; APOLIPOPROTEIN-A-I; SR-BI; HDL RECEPTOR; CHOLESTERYL ESTER;
D O I
10.1097/MED.0000000000000046
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Purpose of reviewTo summarize the recent findings about the roles of scavenger receptor class B type I (SR-BI) in immunity and discuss the underlying mechanisms by which SR-BI prevents immune dysfunctions.Recent findingsSR-BI is well known as a high-density lipoprotein (HDL) receptor playing key roles in HDL metabolism and in protection against atherosclerosis. Recent studies have indicated that SR-BI is also an essential modulator in immunity. SR-BI deficiency in mice causes immune dysfunctions, including increased atherosclerosis, elevated susceptibility to sepsis, impaired lymphocyte homeostasis, and autoimmune disorders. SR-BI exerts its protective roles through a variety of HDL-dependent and HDL-independent mechanisms. SR-BI is also involved in hepatitis C virus cell entry. A deficiency of SR-BI in humanized mice has been shown to decrease hepatitis C virus infectivity.SummarySR-BI regulates immunity via multiple mechanisms and its deficiency causes numerous diseases. A comprehensive understanding of the roles of SR-BI in protection against immune dysfunctions may provide a therapeutic target for intervention against its associated diseases.
引用
收藏
页码:121 / 128
页数:8
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