Niessner A, Goronzy J J, Weyand C M
Lowance Center for Human Immunology, Department of Medicine, Emory University School of Medicine, 101 Woodruff Circle, Atlanta, GA 30322, USA.
Curr Pharm Des. 2007;13(36):3701-10. doi: 10.2174/138161207783018626.
Accumulation of inflammatory cells identifies atherosclerotic plaque at risk for rupture. Typically, activated immune cells occupy the rupture-prone areas of the atherosclerotic lesion. These cells are an appealing therapeutic target for novel strategies of plaque stabilization. Biologic consequences of plaque inflammation ultimately depend not only on the cellular players populating the lesion but also on triggers of immune activation originating from within the plaque or arriving from the circulation, and immune effector mechanisms that mediate cellular damage and plaque destabilization. Recent studies have provided insights into particular immune mechanisms in the atherosclerotic plaque that contribute to plaque vulnerability. This knowledge provides the basis for potential immunomodulatory therapies in cardiovascular disease. These therapeutic approaches can be classified as (1) immunomodulatory effects of existing therapies, (2) therapies targeting inflammatory triggers, and (3) agents inhibiting specific immune mechanisms.
炎症细胞的聚集可识别出有破裂风险的动脉粥样硬化斑块。通常，活化的免疫细胞占据动脉粥样硬化病变中易于破裂的区域。这些细胞是斑块稳定化新策略的一个有吸引力的治疗靶点。斑块炎症的生物学后果最终不仅取决于构成病变的细胞成分，还取决于源自斑块内部或来自循环系统的免疫激活触发因素，以及介导细胞损伤和斑块不稳定的免疫效应机制。最近的研究深入了解了动脉粥样硬化斑块中导致斑块易损性的特定免疫机制。这些知识为心血管疾病潜在的免疫调节治疗提供了基础。这些治疗方法可分为：（1）现有疗法的免疫调节作用；（2）针对炎症触发因素的疗法；（3）抑制特定免疫机制的药物。
