冠心病患者外周血淋巴细胞表面CD1分子的表达及其与血脂的相关性分析
|
摘要
目的:探讨冠状动脉(冠脉)粥样硬化性心脏病(CHD)患者外周血淋巴细胞表面CD1分子的表达特点及其与血脂的相关性。方法:收集2017-11-2018-02于湖北医药学院附属东风医院心内科行冠脉造影检查的患者117例,根据冠脉造影检查发现冠脉狭窄是否≥50%分为CHD组(64例)和对照组(53例)。采用流式细胞术检测2组患者外周血淋巴细胞表面CD1分子的表达情况,并对2组患者的CD1分子、血脂水平进行分析。结果:CHD患者外周血淋巴细胞表面CD1b的表达显著高于对照组,差异有统计学意义(P<0.05);CD1b及CD1d分子的表达与三酰甘油水平呈显著负相关(r=-0.241,P=0.010;r=-0.204,P=0.030)。结论:CD1分子的高表达可能提示其参与了CHD的发病过程,这一机制可能与CD1b的分子结构及其参与的炎症反应相关,且与CD1分子识别并呈递脂质抗原密切相关。
Objective:To investigate the expression characteristics of CD1 molecules on the peripheral blood lymphocytes in patients with coronary atherosclerotic heart disease(CHD)and explore the possible mechanisms of CD1 molecules participating in the pathogenesis of CHD.Method:A total of 117 cases were collected who had received coronary angiography examination in the Department of Cardiology,affiliated Dongfeng Hospital,Hubei University of Medicine,from November 2017 to February 2018.According to the results of coronary angiography,cases were divided into CHD group(64 cases) and control group(53 cases) by whether the coronary artery stenosis was great than 50%.The expression of CD1 molecule on peripheral blood lymphocyte surface was detected by flow cytometry and the levels of CD1 molecule and blood lipid were analyzed.Result:The expression of CD1 b on peripheral blood lymphocyte surface in patients with coronary artery disease is significantly higher than that in the control group(P<0.05).The expression of CD1 b and CD1 d is negatively correlated with triglyceride level(r=-0.241,P=0.010;r=-0.204,P=0.030).Conclusion:The high expression of CD1 b molecule may indicate that this molecule participates in the pathogenesis of CHD and underlying mechanism may include that the molecular structure of CD1 b and its involvement in the inflammatory responses, as well as the recognition and presentation of lipid antigen by CD1 molecule.
Objective:To investigate the expression characteristics of CD1 molecules on the peripheral blood lymphocytes in patients with coronary atherosclerotic heart disease(CHD)and explore the possible mechanisms of CD1 molecules participating in the pathogenesis of CHD.Method:A total of 117 cases were collected who had received coronary angiography examination in the Department of Cardiology,affiliated Dongfeng Hospital,Hubei University of Medicine,from November 2017 to February 2018.According to the results of coronary angiography,cases were divided into CHD group(64 cases) and control group(53 cases) by whether the coronary artery stenosis was great than 50%.The expression of CD1 molecule on peripheral blood lymphocyte surface was detected by flow cytometry and the levels of CD1 molecule and blood lipid were analyzed.Result:The expression of CD1 b on peripheral blood lymphocyte surface in patients with coronary artery disease is significantly higher than that in the control group(P<0.05).The expression of CD1 b and CD1 d is negatively correlated with triglyceride level(r=-0.241,P=0.010;r=-0.204,P=0.030).Conclusion:The high expression of CD1 b molecule may indicate that this molecule participates in the pathogenesis of CHD and underlying mechanism may include that the molecular structure of CD1 b and its involvement in the inflammatory responses, as well as the recognition and presentation of lipid antigen by CD1 molecule.
引文
[1] Kiani AN,Vogel-Claussen J,Arbab-Zadeh A,et al.Semiquantified noncalcified coronary plaque in systemic lupus erythematosus[J].J Rheumatol,2012,39(12):2286-2293.
[2] Vierboom M,Breedveld E,'t Hart BA.New drug discovery strategies for rheumatoid arthritis:a niche for nonhuman primate models to address systemic complications in inflammatory arthritis[J].Expert Opin Drug Disc,2012,7(4):315-325.
[3] Mineo C.Inhibition of nitric oxide and antiphospholipid antibody-mediated thrombosis[J].Curr Rheumatol Rep,2013,15(5):324-336.
[4] McEwen-Smith RM,Salio M,Cerundolo V.CD1d-dependent endogenous and exogenous lipid antigen presentation[J].Curr Opin Immunol,2015,34(5):116-125.
[5] Gensini GG.Gensini GGA more meaningful scoring system for determining the severity of coronary heart diseaseAm J Cardiol 51:606[J].American Journal of Cardiology,1983,51(3):606-606.
[6] Yang Q,Xu J,Ma Q,et al.PRKAA1/AMPKα1-driven glycolysis in endothelial cells exposed to disturbed flow protects against atherosclerosis[J].Nat Commun,2018,9(1):4667.
[7] Wang KC,Yeh YT,Nguyen P,et al.Flow-dependent YAP/TAZ activities regulate endothelial phenotypes and atherosclerosis[J].Proc Natl Acad Sci U S A,2016,113(41):11525-11530.
[8] 徐晓艳,唐啸.HMGB1通过糖基化终末产物受体在动脉粥样硬化发病中的作用[J].临床心血管病杂志,2018,34(9):861-865.
[9] 王洪如,何培菲,吴豫.心肌肌钙蛋白Ⅰ自身抗体和心血管系统疾病[J].临床心血管病杂志,2017,33(7):625-628.
[10] Kasmar AG,van Rhijn I,Cheng TY,et al.CD1b tetramers bind αβ T cell receptors to identify a mycobacterial glycolipid-reactive T cell repertoire in humans[J].J Exp Med,2011,208(9):1741-1747.
[11] Brigl M,Brenner MB.CD1:antigen presentation and T cell function[J].Annu Rev Immunol,2004,22(1):817-890.
[12] Le Nours J,Shahine A,Gras S.Molecular features of lipid-based antigen presentation by group 1 CD1 molecules[J].Semin Cell Dev Biol,2017,11(11):2-10.
[13] Gadola SD,Zaccai NR,Harlos K,et al.Structure of human CD1b with bound ligands at 2.3 A,a maze for alkyl chains[J].Nat Immunol,2002,3(8):721-726.
[14] Cheng TY,Relloso M,Van Rhijn I,et al.Role of lipid trimming and CD1 groove size in cellular antigen presentation[J].EMBO J,2006,25(13):2989-2999.
[15] Elzen PVD,Garg S,León L,et al.Apolipoprotein-mediated pathways of lipid antigen presentation[J].Nature,2005,437(7060):906-910
[16] 朱雁洲,缪海雄,叶椿香,等.糖基化高密度脂蛋白对ApoE(-/-)小鼠颈动脉粥样硬化斑块稳定性的影响[J].临床心血管病杂志,2018,34(9):928-932.
[17] Tupin E,Nicoletti A,Elhage R,et al.CD1d-dependent activation of NKT cells aggravates atherosclerosis[J].J Exp Med,2004,199(3):417-422.
[18] Zeng D,Lee MK,Tung J,et al.Cutting edge:a role for CD1 in the pathogensis of lupus in NZB/NZW mice[J].J Immunol,2000,164(10):5000-5004
[19] Gras S,Van Rhijn I,Shahine A,et al.T cell receptor recognition of CD1b presenting a mycobacterial glycolipid[J].Nat Commun,2016,7(7):13257-13269.
[20] Bagchi S,He Y,Zhang H,et al.CD1b-autoreactive T cells contribute to hyperlipidemia-induced skin inflammation in mice[J].J Clin Invest,2017,127(6):2339-2352.
[21] Taleb S,Tedgui A,Mallat Z.IL-17 and Th17 cells in atherosclerosis:subtle and contextual roles[J].Arterioscler Thromb Vasc Biol,2015,35(2):258-264.
[2] Vierboom M,Breedveld E,'t Hart BA.New drug discovery strategies for rheumatoid arthritis:a niche for nonhuman primate models to address systemic complications in inflammatory arthritis[J].Expert Opin Drug Disc,2012,7(4):315-325.
[3] Mineo C.Inhibition of nitric oxide and antiphospholipid antibody-mediated thrombosis[J].Curr Rheumatol Rep,2013,15(5):324-336.
[4] McEwen-Smith RM,Salio M,Cerundolo V.CD1d-dependent endogenous and exogenous lipid antigen presentation[J].Curr Opin Immunol,2015,34(5):116-125.
[5] Gensini GG.Gensini GGA more meaningful scoring system for determining the severity of coronary heart diseaseAm J Cardiol 51:606[J].American Journal of Cardiology,1983,51(3):606-606.
[6] Yang Q,Xu J,Ma Q,et al.PRKAA1/AMPKα1-driven glycolysis in endothelial cells exposed to disturbed flow protects against atherosclerosis[J].Nat Commun,2018,9(1):4667.
[7] Wang KC,Yeh YT,Nguyen P,et al.Flow-dependent YAP/TAZ activities regulate endothelial phenotypes and atherosclerosis[J].Proc Natl Acad Sci U S A,2016,113(41):11525-11530.
[8] 徐晓艳,唐啸.HMGB1通过糖基化终末产物受体在动脉粥样硬化发病中的作用[J].临床心血管病杂志,2018,34(9):861-865.
[9] 王洪如,何培菲,吴豫.心肌肌钙蛋白Ⅰ自身抗体和心血管系统疾病[J].临床心血管病杂志,2017,33(7):625-628.
[10] Kasmar AG,van Rhijn I,Cheng TY,et al.CD1b tetramers bind αβ T cell receptors to identify a mycobacterial glycolipid-reactive T cell repertoire in humans[J].J Exp Med,2011,208(9):1741-1747.
[11] Brigl M,Brenner MB.CD1:antigen presentation and T cell function[J].Annu Rev Immunol,2004,22(1):817-890.
[12] Le Nours J,Shahine A,Gras S.Molecular features of lipid-based antigen presentation by group 1 CD1 molecules[J].Semin Cell Dev Biol,2017,11(11):2-10.
[13] Gadola SD,Zaccai NR,Harlos K,et al.Structure of human CD1b with bound ligands at 2.3 A,a maze for alkyl chains[J].Nat Immunol,2002,3(8):721-726.
[14] Cheng TY,Relloso M,Van Rhijn I,et al.Role of lipid trimming and CD1 groove size in cellular antigen presentation[J].EMBO J,2006,25(13):2989-2999.
[15] Elzen PVD,Garg S,León L,et al.Apolipoprotein-mediated pathways of lipid antigen presentation[J].Nature,2005,437(7060):906-910
[16] 朱雁洲,缪海雄,叶椿香,等.糖基化高密度脂蛋白对ApoE(-/-)小鼠颈动脉粥样硬化斑块稳定性的影响[J].临床心血管病杂志,2018,34(9):928-932.
[17] Tupin E,Nicoletti A,Elhage R,et al.CD1d-dependent activation of NKT cells aggravates atherosclerosis[J].J Exp Med,2004,199(3):417-422.
[18] Zeng D,Lee MK,Tung J,et al.Cutting edge:a role for CD1 in the pathogensis of lupus in NZB/NZW mice[J].J Immunol,2000,164(10):5000-5004
[19] Gras S,Van Rhijn I,Shahine A,et al.T cell receptor recognition of CD1b presenting a mycobacterial glycolipid[J].Nat Commun,2016,7(7):13257-13269.
[20] Bagchi S,He Y,Zhang H,et al.CD1b-autoreactive T cells contribute to hyperlipidemia-induced skin inflammation in mice[J].J Clin Invest,2017,127(6):2339-2352.
[21] Taleb S,Tedgui A,Mallat Z.IL-17 and Th17 cells in atherosclerosis:subtle and contextual roles[J].Arterioscler Thromb Vasc Biol,2015,35(2):258-264.