Kodama M, Zhang S, Hanawa H, Shibata A
First Department of Internal Medicine, Niigata University School of Medicine, Japan.
Clin Exp Immunol. 1992 Nov;90(2):330-5. doi: 10.1111/j.1365-2249.1992.tb07951.x.
The pathogenesis of giant cell myocarditis remains unclear. Subsets of inflammatory infiltrating cells may reflect the pathogenesis and etiology of the disease. Therefore, we examined subsets of infiltrating mononuclear cells in the heart of the rat with experimental giant cell myocarditis. Lewis rats were immunized with cardiac myosin in Freund's complete adjuvant (FCA). Severe myocarditis characterized by congestive heart failure and multinucleated giant cells were elicited. The lesions were composed of predominant mononuclear cells, polymorphonuclear neutrophils and fragments of degenerated myocardial fibres. The subsets of infiltrating mononuclear cells were investigated using MoAbs against rat CD4+ T cell (W3/25), CD8+ T cell (CX8), B cell (OX33) and macrophage (OX42). By serial examination, bound immunoglobulin could only be found on degenerated myocardial fibres. In this model, most infiltrating mononuclear cells were composed of macrophages and CD4+ T cells. The frequencies of macrophages and CD4+ T cells were 73.7% and 13.8%, respectively. CD8+ T cells were scarce and B cells were rare in the lesions. The frequencies of CD8+ T cells and B cells were 4.5% and 0.4%, respectively. The dominance of macrophages and CD4+ T cells was the constant finding among the sites of the lesions and throughout the course of the disease. These characteristic subsets of infiltrating cells were in contrast to those of murine viral myocarditis which were mainly composed of natural killer (NK) cells and CD8+ T cells. Clarifying the subsets of infiltrating cells in myocarditis may contribute to differential diagnosis of myocarditis between viral and autoimmune types. From this study, the pathogenesis of experimental autoimmune giant cell myocarditis seemed to be closely related to CD4+ T cells and macrophages.
巨细胞性心肌炎的发病机制尚不清楚。炎性浸润细胞亚群可能反映了该疾病的发病机制和病因。因此，我们检测了实验性巨细胞性心肌炎大鼠心脏中浸润的单核细胞亚群。将Lewis大鼠用弗氏完全佐剂（FCA）中的心肌肌凝蛋白免疫。引发了以充血性心力衰竭和多核巨细胞为特征的严重心肌炎。病变主要由单核细胞、多形核中性粒细胞和变性心肌纤维碎片组成。使用抗大鼠CD4 + T细胞（W3/25）、CD8 + T细胞（CX8）、B细胞（OX33）和巨噬细胞（OX42）的单克隆抗体研究浸润单核细胞的亚群。通过连续检查，仅在变性心肌纤维上发现结合的免疫球蛋白。在该模型中，大多数浸润的单核细胞由巨噬细胞和CD4 + T细胞组成。巨噬细胞和CD4 + T细胞的频率分别为73.7%和13.8%。病变中CD8 + T细胞稀少，B细胞罕见。CD8 + T细胞和B细胞的频率分别为4.5%和0.4%。巨噬细胞和CD4 + T细胞的优势在病变部位和疾病全过程中均持续存在。这些浸润细胞的特征性亚群与主要由自然杀伤（NK）细胞和CD8 + T细胞组成的小鼠病毒性心肌炎不同。阐明心肌炎中浸润细胞的亚群可能有助于鉴别病毒性和自身免疫性心肌炎。从本研究来看，实验性自身免疫性巨细胞性心肌炎的发病机制似乎与CD4 + T细胞和巨噬细胞密切相关。
