Das S K, Cassidy J T, Huber S A
Heart Vessels Suppl. 1985;1:205-8. doi: 10.1007/BF02072394.
Although several immunologic parameters have been found to be abnormal, their precise relationship to the cause of the disease remains unclear. It is believed that a virus initiating a bout of myocarditis may play a role in the perpetuation of the chronic phase, probably via immunologic mediation. A selection acquired defect or damage to a subpopulation of suppressor T lymphocytes is possible, providing the basis for the development of an autoimmune disorder. Studies in mice have shown a clear link between active viral myocarditis and the subsequent development of cardiomyopathy. However, the trigger mechanism that initiates the cardiomyopathy is still elusive. Specific antigens, possibly altered virus or damaged cardiac tissue, may be playing the role of the "hidden or cloistered" antigen in eliciting the immunologic reactions through a cytotoxic T-cell mechanism. Identification and isolation of the specific "antigen" in question could resolve the dilemmas about the immunopathogenesis of cardiomyopathy in humans.
尽管已发现多项免疫参数异常，但其与该疾病病因的确切关系仍不清楚。据信，引发心肌炎发作的病毒可能在慢性期的持续发展中起作用，可能是通过免疫介导。有可能是抑制性T淋巴细胞亚群出现选择性获得性缺陷或损伤，为自身免疫性疾病的发展提供了基础。对小鼠的研究表明，活动性病毒性心肌炎与随后的心肌病发展之间存在明确联系。然而，引发心肌病的触发机制仍然难以捉摸。特定抗原，可能是改变的病毒或受损的心脏组织，可能在通过细胞毒性T细胞机制引发免疫反应中扮演“隐藏或隔离”抗原的角色。识别并分离出相关的特定“抗原”，可能会解决人类心肌病免疫发病机制方面的难题。
