Izumi T, Hanawa H, Saeki M, Kodama M
First Department of Internal Medicine, Niigata University School of Medicine, Japan.
Mol Cell Biochem. 1993 Feb 17;119(1-2):67-71. doi: 10.1007/BF00926855.
Concerning cardiac contractile proteins, antigenicity and myocardiotogenicity were discussed. In normal states, these proteins are immunologically tolerant, and can not provoke any heart-specific disease. Why the proteins can provoke such lethal autoimmune myocarditis has not been completely elucidated. Shortly after cardiac infection or myocardial ischemia, these proteins may work as the antigen for the autoimmune myocarditis. First of all, the role of cardiac myosin has been strongly emphasized. But, the antigen determinants: epitope proteins remain unclear. Either cross-activity to the streptococcal M protein and/or the alpha-helical coiled-coil protein may be an important factor to determine antigenicity. In this autoimmune myocarditis, the roles of T-lymphocyte and cardiac dendritic cell are noticeable. Through further study on the relation between antigen epitope and the infectious agents in the heart; on cardio-cytotoxicity of the T-lymphocyte and on the precise contribution of cardiac dendritic cells, this autoimmune myocarditis will be more clarified.
关于心脏收缩蛋白,讨论了其抗原性和心肌生成性。在正常状态下,这些蛋白具有免疫耐受性,不会引发任何心脏特异性疾病。这些蛋白为何会引发如此致命的自身免疫性心肌炎尚未完全阐明。在心脏感染或心肌缺血后不久,这些蛋白可能作为自身免疫性心肌炎的抗原。首先,心脏肌球蛋白的作用得到了强烈强调。但是,抗原决定簇:表位蛋白仍不清楚。与链球菌M蛋白和/或α-螺旋卷曲螺旋蛋白的交叉活性可能是决定抗原性的重要因素。在这种自身免疫性心肌炎中,T淋巴细胞和心脏树突状细胞的作用值得注意。通过进一步研究心脏中抗原表位与感染因子之间的关系;T淋巴细胞的心脏细胞毒性以及心脏树突状细胞的确切作用,这种自身免疫性心肌炎将得到更清晰的阐明。