Leukocyte ABC-transporter A1 and LDL receptor play independent roles in atherosclerosis:the potential contribution of T cells
作者单位：Department of Pathology and PathophysiologySoochow University Division of BiopharmaceuticsLeiden/Amsterdam Center for Drug ResearchLeiden University Institute of Biology and Medical SciencesSoochow University
会议名称：《第九届全国免疫学学术大会》
会议日期：2014年
学科分类：1001[医学-基础医学(可授医学、理学学位)] 100102[医学-免疫学] 10[医学]
关 键 词：LDL receptor ABCA1 lymphocytosis T lymphocytes atherosclerosis
摘 要：Background:LDL receptor(LDLr)and ABC-transporter A1(ABCA1)are two distinct players in cellular cholesterol *** recognizes apoprotein B100 and apoE in lipoproteins to mediate the uptake of cholesterol,while ABCA1 promotes excess cholesterol efttux to apoprotein ***:The present study aims to investigate whether LDLr deficiency influences the atheroprotective effects of leukocyte ABCA1 in *** and Results:LDLr-/-mice were transplanted with bone marrow from LDLr/ABCA1mice,LDLr/ABCA1/-mice,and their respective *** leukocyte ABCA1 deficiency reduced plasma cholesterol levels,after 8weeks of Western-type diet feeding,animals transplanted with LDLr/ABCA1and LDLr/ABCA1bone marrow developed 1.6-fold(p0.01)and 1.4-fold(p0.05)larger lesions,compared to their respective *** clearly indicates that the atheroprotection of leukocyte ABCA1 is not affected by ***-way ANOVA analysis also demonstrated that deletion of the leukocyte LDLr reduced lesion development(p0.001),especially in the absence of leukocyte ***,leukocyte LDLr deficiency did not affect monocytosis,recruitment of moncocytes and macrophage foam cell ***,the deletion of leukocyte ABCA1 did reduce lymphocytosis and recruitment of T cells into the adventitia of lesions,associated with smaller lesion size in LDLr/ABCA1transplanted mice,indicating the potential contribution of lymphocytosis and recruitment ofT cells to ***:Leukocyte LDLr deficiency does not affect the atheroprotective effects of leukocyte ***,suppression of lymphocytosis and recruitment of T cells in the adventitia could contribute to the atheroprotection of Leukocyte LDLr deficiency and ABCA1.