冠心病患者外周血树突状细胞前体的数量变化及意义

目的:比较各种类型冠心病患者外周循环树突状细胞(dendritic cells,DCs)前体及其亚型髓系DCs(myeloid DCs,mDCs)和淋巴系DCs(plasmacytoid DCs,pDCs)的数量,探讨DCs参与的炎性免疫反应在冠心病发生发展中的作用。方法:入选冠脉狭窄50%的胸痛患者18例(N组)、稳定型冠心病(stable coronary artery disease,SCAD)患者17例(SCAD组)、不稳定型心绞痛(unstable angina,UA)患者15例(UA组)、非ST段抬高型心肌梗死(non-ST-elevation myocardial infarction,NSTEMI)患者15例(NSTEMI组)、ST段抬高型心肌梗死(ST-elevation myocardial infarction,STEMI)患者16例(STEMI组)。以流式细胞仪四色分析法计数5组外周循环DCs前体及亚型的比例及绝对数,NSTEMI和STEMI患者入院1周后随访外周循环DCs水平。结果:相比N组,UA患者外周循环mDCs和mDC1s明显增多;NSTEMI和STEMI患者外周循环mDCs和mDC1s明显减少;STEMI患者pDCs亦明显减少;SCAD患者无明显差异。入院1周后NSTEMI和STEMI患者外周循环mDCs、mDC1s、pDCs较入院时均明显升高。结论:冠心病发展过程中DCs可能使Th1应答增强,从而参与斑块的不稳定和破裂过程。

Precursor Frequency of Circulating Dendritic Cells in Patients with Coronary Artery Disease

Objective： The frequency of circulating dendritic cells （DCs） precursors of different subsets in coronary artery disease （CAD） patients and healthy people were studied. Methods：Using flow cytometry, circulating DC precursors and subsets were detected in patients with chest pain whose coronary artery stenosis〈50% （Group N, n = 18）,CAb patients with stable coronary artery disease （SCAb, n = 17）, unstable angina （UA, n = 15）, non-ST-elevation myocardial infarction （ NSTEMI, n = 15） and ST-elevation myocardial infarction （STEMI, n = 16）. Peripheral-blood DCs in NSTEMI group and STEMI group were followed up one week after admission. Results： Compared with Group N, circulating mDCs and mbCls were significantly increased in patients with UA, but significantly decreased in NSTEMI group and STEMI group. In contrast, mDCs and mbCls were not significantly altered in SCAD group. The number and the proportion of pDCs precursors in peripheral circulating white cells were significantly decreased in STEMI group. The number and the proportion of mDCs, mDCls, pbCs in peripheral circulation white cells were significantly increased one week after admission in NSTEMI group and STEMI group. Conclusions： DCs may be recruited in the enhanced Th1 response in the development of CAD. DCs may take part in the instability and rupture of the plaques.