Izumi T, Kodama M, Shibata A
First Department of Internal Medicine, Niigata University School of Medicine, Japan.
Eur Heart J. 1991 Aug;12 Suppl D:166-8. doi: 10.1093/eurheartj/12.suppl_d.166.
To identify a cardiac protein that could cause a serious autoimmune myocarditis, membranous proteins and myosin as antigens were investigated. In mice immunized with membranous proteins, the lesions induced were limited on the histological level. On the other hand, in Lewis rats immunized with cardiac myosin, serious myocarditis was induced. Every rat showed evidence of heart failure which was fatal in a few. Histology disclosed extensive cell infiltrates and myocardial necrosis. Among those lesions, giant cells were present. This myocarditis could be also transferred adoptively by lectin-activated spleen cells, T-lymphocytes, but not by IgG fraction. Thus, cardiac myosin can induce autoimmune giant cell myocarditis in Lewis rats.
为了鉴定一种可能导致严重自身免疫性心肌炎的心脏蛋白，对作为抗原的膜蛋白和肌球蛋白进行了研究。在用膜蛋白免疫的小鼠中，诱导的病变在组织学水平上有限。另一方面，在用心脏肌球蛋白免疫的Lewis大鼠中，诱导出了严重的心肌炎。每只大鼠都出现了心力衰竭的迹象，少数大鼠因此死亡。组织学检查显示有广泛的细胞浸润和心肌坏死。在这些病变中，存在巨细胞。这种心肌炎也可以通过凝集素激活的脾细胞、T淋巴细胞进行过继转移，但不能通过IgG组分进行。因此，心脏肌球蛋白可在Lewis大鼠中诱导自身免疫性巨细胞心肌炎。
