中文摘要：

目的：探讨急性冠状动脉综合征（ACS）患者外周血CD4^＋CD28^nullT细胞和CD4^＋CD28^nullT细胞上电压依赖性钾离子通道（Kvl．3）和钙依赖激活的钾离子通道（IKcal）的表达。方法：入选对象共75例，分为3组：其中ACS组27例，稳定型心绞痛组20例，对照组28例。分离外周血单个核细胞（PBMCs），用ELISA法测定PBMCs中NF-κB的活性，流式细胞仪计数CD4^＋CD28^nullT细胞占CD4^＋T细胞的比例。免疫荧光染色标记结合膜片钳技术记录ACS组CD4^＋CD28^nullT细胞和CD4^＋CD28^nullT细胞上Kvl．3和IKCal的电流，计算单细胞上通道的数目。结果：ACS组NF-κB的活性和CD4^＋CD28^nullT细胞的比例显著高于稳定型心绞痛组和对照组（P〈0．05）。NF-κB的活性和CD4^＋CD28^nullT细胞的比例具有正相关关系（r=0．369，P〈0．05）。CD4^＋CD28^nullT细胞上Kv1．3的数目和电流密度显著高于CD4^＋CD28^＋T细胞（P〈0．05）。CD4^＋CD28^nullT细胞、CD4^＋CD28^＋T细胞上IKCal的数目差异无统计学意义（P〉0．05）。结论：Kvl．3通道对CD4^＋CD28^nullT细胞的功能具有重要作用，Kvl．3通道有可能成为AS治疗的新靶点。

英文摘要：

Objective：To investigate the expression of voltage-gated potassium channel 1.3（Kvl. 3） and calcium-activated potassium channel （IKCal） on the subset of CD4^＋T lymphocytes in peripheral blood of patients with acute coronary syndrome（ACS）. Method： Peripheral blood mononuclear cells （PBMCs） were obtained from 27 patients with ACS, 20 patients with stable angina and 28 matched controls. The proportion of CD4^＋CD28^nullT lymphocytes was detected by flow cytometry. The activity of nuclear factor kappaB in PBMCs was quantified in an ELISA based essays. To calculate the number of the channel on a single cell the current of Kvl. 3 and IKCal in T cells were recorded by patch clamp technique combined with immunofluorescence. Result：The proportion of CD4^＋CD28^null T lymphocytes and the activity of NF-κB were significantly higher in patients with ACS than in the other groups （P〈0. 05）. There was a positive correlation between the number of CD4^＋CD28^null T lymphocyte and the activity of NF-κB（r=0. 369,P〈0.05）. Patch clamp revealed that the number of IKCal in the two subsets of CD4^＋T cell was similar, Whereas the expression of Kvl. 3 appeared to be great different. CD4^＋CD28^nullT lymphocyte had far more Kvl. 3 channels and higher current density than CD4^＋ CD28^＋ T lymphocyte （P〈0.05）. Conelusion：CD4^＋CD28^nullT lymphocytes in patients with ACS exhibit Kvl. 3^ high iKCal^low phenotype, which may confer the possibility of using Kvl. 3 blocker as a new therapy for atherosclerosis.