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Immunohistochemical characterization of infiltrating mononuclear cells in the rat heart with experimental autoimmune giant cell myocarditis.

机译:实验性自身免疫性巨细胞心肌炎在大鼠心脏中浸润的单核细胞的免疫组织化学表征。

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摘要

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.
机译:巨细胞心肌炎的发病机制仍不清楚。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,我们检查了实验性巨细胞心肌炎大鼠心脏中浸润的单核细胞的子集。用弗氏完全佐剂(FCA)中的心肌肌球蛋白免疫Lewis大鼠。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。病变由主要的单核细胞,多形核中性粒细胞和变性心肌纤维碎片组成。使用针对大鼠CD4 + T细胞(W3 / 25),CD8 + T细胞(CX8),B细胞(OX33)和巨噬细胞(OX42)的MoAb,研究了浸润的单核细胞的亚群。通过系列检查,结合的免疫球蛋白只能在变性的心肌纤维上发现。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,而B细胞很少。 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细胞的优势是在病变部位和整个疾病过程中不断发现的。这些浸润细胞的特征性子集与鼠病毒性心肌炎的特征性子集相反,后者主要由自然杀伤(NK)细胞和CD8 + T细胞组成。澄清心肌炎中浸润细胞的亚群可能有助于病毒性和自身免疫性类型之间心肌炎的鉴别诊断。根据这项研究,实验性自身免疫性巨细胞心肌炎的发病机制似乎与CD4 + T细胞和巨噬细胞密切相关。

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