Seko Y, Yagita H, Okumura K, Yazaki Y
Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
J Pathol. 1996 Dec;180(4):450-4. doi: 10.1002/(SICI)1096-9896(199612)180:4<450::AID-PATH693>3.0.CO;2-5.
Cell-mediated autoimmunity has been strongly implicated in the pathogenesis of the myocardial cell damage involved in viral myocarditis. Using a murine model of acute myocarditis caused by Coxsackievirus B3 (CVB3), perforin-expressing killer cells have been shown to infiltrate the heart, and intercellular adhesion molecular-1 (ICAM-1) together with major histocompatibility complex (MHC) antigen was induced on myocardial cells in acute viral myocarditis. To clarify the immunological mechanisms in more detail, the expression of vascular cell adhesion molecular-1 (VCAM-1) has been examined in the heart of acute myocarditis and on cultured cardiac myocytes treated with interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha). The effects of in vivo antibody treatment to VCAM-1 on myocardial damage involved in acute myocarditis were also analysed. CVB3-induced myocarditis resulted in enhanced expression of VCAM-1 on myocardial cells. VCAM-1 expression was also induced on cultured cardiac myocytes by treatment with IFN-gamma and TNF-alpha. The in vivo antibody treatment to VCAM-1 decreased the myocardial damage to some extent, but the effects were not statistically significant. These data suggest that the expression of VCAM-1 on myocardial cells may play at least a partial role in the myocardial damage involved in acute viral myocarditis.
细胞介导的自身免疫在病毒性心肌炎所致心肌细胞损伤的发病机制中具有重要作用。利用柯萨奇病毒B3（CVB3）诱发的急性心肌炎小鼠模型，已证实表达穿孔素的杀伤细胞浸润心脏，且在急性病毒性心肌炎中，心肌细胞上可诱导表达细胞间黏附分子-1（ICAM-1）以及主要组织相容性复合体（MHC）抗原。为更详细地阐明免疫机制，研究人员检测了急性心肌炎小鼠心脏以及经γ干扰素（IFN-γ）和肿瘤坏死因子-α（TNF-α）处理的培养心肌细胞中血管细胞黏附分子-1（VCAM-1）的表达情况。同时还分析了体内给予抗VCAM-1抗体对急性心肌炎所致心肌损伤的影响。CVB3诱发的心肌炎导致心肌细胞上VCAM-1表达增强。用IFN-γ和TNF-α处理培养的心肌细胞也可诱导VCAM-1表达。体内给予抗VCAM-1抗体在一定程度上减轻了心肌损伤，但效果无统计学意义。这些数据表明，心肌细胞上VCAM-1的表达可能在急性病毒性心肌炎所致心肌损伤中至少起部分作用。
