Penninger J M, Bachmaier K
Amgen Institute, Ontario Cancer Institute, and Department of Medical Biophysics, University of Toronto, Toronto, Ontario M5G 2C1, Canada.
J Infect Dis. 2000 Jun;181 Suppl 3:S498-504. doi: 10.1086/315613.
Heart disease is the most prevalent cause of morbidity and mortality in rich countries. Multiple pathogens are epidemiologically linked to human heart disease, and autoinflammatory responses to heart-specific epitopes revealed to the host's immune system (e.g., due to the cytopathic effects of cardiotropic viruses) or attacked by autoaggresive lymphocytes activated by mimicking peptides present in bacteria may be causative in the pathogenesis of chronic inflammatory cardiomyopathy. The experimental system of murine chronic autoimmune myocarditis has been used to analyze aspects of the host immune response. This review presents insights gained by use of this murine model system into molecular mechanisms governing activation of autoaggressive lymphocytes, target organ susceptibility, and cardiopathogenic epitope mapping and discusses mimicking endogenous epitopes found in pathogens.
在富裕国家，心脏病是发病率和死亡率最高的病因。多种病原体在流行病学上与人类心脏病相关，对宿主免疫系统所暴露的心脏特异性表位产生的自身炎症反应（例如，由于嗜心性病毒的细胞病变效应），或被模仿细菌中存在的肽段激活的自身攻击性淋巴细胞攻击，可能是慢性炎症性心肌病发病机制的病因。小鼠慢性自身免疫性心肌炎的实验系统已被用于分析宿主免疫反应的各个方面。本综述介绍了通过使用该小鼠模型系统在控制自身攻击性淋巴细胞激活、靶器官易感性和心脏致病表位定位的分子机制方面所获得的见解，并讨论了模仿病原体中发现的内源性表位。
