Ayada Kiyoshi, Yokota Kenji, Kobayashi Kazuko, Shoenfeld Yehuda, Matsuura Eiji, Oguma Keiji
Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, 700-8558, Japan.
Clin Rev Allergy Immunol. 2009 Aug;37(1):44-8. doi: 10.1007/s12016-008-8097-7.
The immune response against heat shock protein 60 (HSP60) derived from pathogens causing chronic infections is thought to be an important pro-atherogenic mechanism because high serum levels of antibodies against HSP60 have been associated with atherosclerotic diseases, such as coronary artery diseases, or cerebro-vascular events. Furthermore, the presence of HSP60-specific T lymphocytes in circulation may increase the risk of atherosclerosis. Our recent in vitro and in vivo studies have also shown an association of Helicobacter pylori-HSP60 (Hp-HSP60) specific Th1 immune responses elicited by H. pylori infection with the progression of atherosclerosis in a hyperlipidemic mouse model. These Th1 dominant immune responses may cross-react with endogenous HSP60 expressed on stressed cells of the vascular endothelium, likely due to molecular mimicry. However, the exact mechanisms by which endothelial cells display their HSP60 molecule or present HSP60 antigenic epitopes on the surface are still unclear.
针对源自引起慢性感染的病原体的热休克蛋白60（HSP60）的免疫反应被认为是一种重要的促动脉粥样硬化机制，因为血清中抗HSP60抗体的高水平与动脉粥样硬化疾病有关，如冠状动脉疾病或脑血管事件。此外，循环中存在HSP60特异性T淋巴细胞可能会增加动脉粥样硬化的风险。我们最近的体外和体内研究还表明，幽门螺杆菌感染引发的幽门螺杆菌热休克蛋白60（Hp-HSP60）特异性Th1免疫反应与高脂血症小鼠模型中动脉粥样硬化的进展有关。这些Th1主导的免疫反应可能与血管内皮应激细胞上表达的内源性HSP60发生交叉反应，这可能是由于分子模拟。然而，内皮细胞展示其HSP60分子或在表面呈递HSP60抗原表位的确切机制仍不清楚。
