Cardiovascular Division, King's College London, London, UK.
Autoimmunity. 2009 Nov;42(7):627-33. doi: 10.1080/08916930903002529.
The endothelium of the vessel wall as a barrier between blood and the subendothelial matrix proteins is essential for preventing thrombus formation and subsequent atherosclerosis development. Atherosclerosis is an inflammatory disease in which immune and autoimmune mechanisms are involved. Recently, it was demonstrated that endothelial cells in the vessel wall can be damaged not only by classic risk factors, such as hyperlipidemia, smoking and disturbed blood flow, but also (auto)immune reactions to autoantigens present in the cell surface, among which heat shock protein 60 (HSP60) was mostly studied. HSP60 normally located in mitochondria can be translocated into the cell member in response to stress stimuli. Meanwhile, autoantibodies against HSP60 are present in most subjects, especially patients with heart attack and stroke. These autoantibodies may bind to HSP60 expressed in endothelial cells resulting in the cell damage, subsequently initiating the formation of atherosclerotic lesions. Based on the recent progress in the research field, the present review will update the mechanisms of immune response to endothelial cells by which cell damage can initiate the development of atherosclerosis.
血管壁内皮作为血液和血管下基质蛋白之间的屏障，对于防止血栓形成和随后的动脉粥样硬化发展至关重要。动脉粥样硬化是一种炎症性疾病，其中涉及免疫和自身免疫机制。最近，已经证明血管壁中的内皮细胞不仅可以被经典的风险因素（如高血脂、吸烟和血流紊乱）损伤，还可以被自身抗原的（自身）免疫反应损伤，其中热休克蛋白 60（HSP60）是研究最多的一种。HSP60 通常位于线粒体中，在应激刺激下可以被转移到细胞质中。同时，针对 HSP60 的自身抗体存在于大多数患者中，尤其是心脏病发作和中风患者。这些自身抗体可能与内皮细胞中表达的 HSP60 结合，导致细胞损伤，随后启动动脉粥样硬化病变的形成。基于该研究领域的最新进展，本综述将更新对内皮细胞的免疫反应机制，该机制可以通过细胞损伤引发动脉粥样硬化的发展。
