Izumi T, Kodama M, Fujiwara M
Department of First Internal Medicine, Niigata University School of Medicine, Japan.
Jpn Circ J. 1991 Nov;55(11):1138-43. doi: 10.1253/jcj.55.1138.
In this paper, the ability of human cardiac myosin to provoke autoimmune myocarditis was investigated. Myosin fractions were immunized into A.SW. mice, Lewis rats or Hartley guinea pigs. All of the immunized rats displayed overt symptoms of myocarditis and, in a few cases, died from it. The hearts of these rats were enlarged and discolored. Histologically, the muscles of the heart were characterized by remarkable cell infiltration, extensive myofiber necrosis and the appearance of polynuclear giant cells. Neither mice nor guinea pigs showed such disease profile. In this novel experimental model, the disease state was transferable by T lymphocytes. Thus, cardiac myosin was shown to provoke muscle cell damage through a T cell mediated autoimmune process.
在本文中，对人心脏肌球蛋白引发自身免疫性心肌炎的能力进行了研究。将肌球蛋白组分免疫接种到A.SW.小鼠、刘易斯大鼠或哈特利豚鼠体内。所有免疫接种的大鼠均表现出明显的心肌炎症状，少数情况下死于该病。这些大鼠的心脏增大且变色。组织学上，心脏肌肉的特征是明显的细胞浸润、广泛的肌纤维坏死以及多核巨细胞的出现。小鼠和豚鼠均未表现出这种疾病特征。在这个新的实验模型中，疾病状态可通过T淋巴细胞转移。因此，心脏肌球蛋白被证明可通过T细胞介导的自身免疫过程引发肌肉细胞损伤。
