Kodama M, Matsumoto Y, Fujiwara M
First Department of Internal Medicine, Niigata University School of Medicine, Japan.
Circulation. 1992 May;85(5):1918-26. doi: 10.1161/01.cir.85.5.1918.
To elucidate the mechanisms of immune-related myocardial injuries, we examined whether autoimmune myocarditis was passively transferable by use of humoral or cellular factors.
Active myocarditis was elicited in Lewis rats by immunization with human cardiac myosin fraction in complete Freund's adjuvant. This experimental myocarditis was characterized by macroscopic features such as pericardial effusion, enlargement of the heart, and gray discoloration of the cardiac surface. Histologically, extensive myocardial necrosis and numerous inflammatory cell infiltrations were observed. Interestingly, multinucleated giant cells were frequently observed in the lesions. Transfer of the disease by the humoral factor was examined by use of fresh sera and immunoglobulin fraction of pooled sera from rats with severe myocarditis, and transfer by the cellular factor was tested by use of spleen cells and lymph node cells from the diseased rats. When naive Lewis rats were given 15.75 mg of immunoglobulin fraction, no particular change was observed in the hearts. Fresh sera also could not elicit myocarditis in recipient rats. In contrast, intravenous injection of spleen cells or lymph node cells that were cultured for 3 days in the presence of 1 microgram/ml of concanavalin A elicited severe myocarditis. The macroscopic and microscopic findings of passively transferred myocarditis are essentially the same as those found in actively induced myocarditis. Multinucleated giant cells were also observed in the lesions of transferred myocarditis.
This study demonstrates direct evidence for in vivo lymphocyte-mediated myocardial injuries.
为阐明免疫相关心肌损伤的机制，我们研究了自身免疫性心肌炎是否可通过体液或细胞因子被动转移。
用完全弗氏佐剂中的人心脏肌球蛋白组分免疫Lewis大鼠诱发活动性心肌炎。这种实验性心肌炎的特征包括心包积液、心脏增大和心脏表面颜色变灰等宏观特征。组织学上，观察到广泛的心肌坏死和大量炎性细胞浸润。有趣的是，在病变中经常观察到多核巨细胞。通过使用来自重症心肌炎大鼠的新鲜血清和混合血清的免疫球蛋白组分来检测疾病通过体液因子的转移，并通过使用患病大鼠的脾细胞和淋巴结细胞来测试疾病通过细胞因子的转移。当给未免疫的Lewis大鼠注射15.75 mg免疫球蛋白组分时，心脏未观察到特殊变化。新鲜血清也不能在受体大鼠中诱发心肌炎。相反，静脉注射在1微克/毫升伴刀豆球蛋白A存在下培养3天的脾细胞或淋巴结细胞可诱发重症心肌炎。被动转移的心肌炎的宏观和微观表现与主动诱导的心肌炎基本相同。在转移的心肌炎病变中也观察到多核巨细胞。
本研究证明了体内淋巴细胞介导心肌损伤的直接证据。
