免疫机制参与的慢性炎症反应是粥样硬化发生和发展的重要因素。CD4+ T细胞是血管炎症反应主要效应细胞。与经典CD4+CD28+ T细胞不同，CD4+CD28null T细胞是一种异常细胞，其异常增殖并分泌大量炎症因子，导致炎症恶化和疾病进展。目前认为 CD4+CD28+ T细胞受慢性炎症刺激后转化为CD4+CD28null T细胞。探讨CD4+CD28+/CD28null T细胞表型转化的调控，对控制炎症反应转归及稳定动脉粥样硬化斑块具有重要意义。Kv1.3和KCa3.1钾通道通过调控T细胞内钙信号在T细胞活化和功能中发挥关键作用。我们前期研究发现急性冠脉综合征患者活化的CD4+CD28null T细胞，Kv1.3通道的表达显著增高。本课题中，我们拟探讨Kv1.3与KCa3.1通道在CD4+CD28+/CD28null T细胞免疫表型转化中的作用，进而对动脉粥样硬化斑块稳定性的影响及机制。

Chronic inflammation process that involves the immune system plays a significant role in the initiation and progression of atherosclerosis. CD4+ T cells are suggested to be the major effector cells which mediate vascular inflammation. CD4+CD28null T cells, different from classical CD4+CD28+ T cells, are characterized by the production of high level of pro-in?ammatory factors, which accelerate the inflammation-mediated progressive atherosclerosis. CD4+CD28null T cells are considered to be derived from the same precursors as CD28+ as a result of chronic inflammatory stimulation. Investigation of the mechanism under the CD4+CD28+/CD28null T cells transformation is very important for control inflammatory response and stabilizing plaque. Kv1.3 and KCa3.1 channels，two major potassium channels regulating Ca2+ signal in T cells, play key roles in T cells activation and function. Our previous study has proved that CD4+CD28null T cells from acute coronary syndrome patients express high level of Kv1.3 channel. In this project, we will investigate the role and mechanism of Kv1.3 and KCa3.1 channels in the CD4+CD28+/CD28null T cells transformation and plaque stabilization.