柯萨奇病毒b3诱导MHC ii型缺陷小鼠心肌炎。

Journal of human virology Pub Date : 1999-03-01
C Leipner, M Borchers, I Merkle, A Stelzner
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引用次数: 0

摘要

目的:研究柯萨奇病毒B3 (CVB3)诱导的心肌炎在具有相同遗传背景的免疫活性C57BL/6和MHC II类敲除小鼠中的发病机制。研究设计/方法:我们分析了心肌损伤的组织学和免疫组织学、复制病毒滴度和疾病早期和晚期的抗体反应。结果:cvb3感染C57BL/6小鼠出现急性心肌炎,自行愈合,病毒消除,抗cvb3 IgM/IgG产生,中和抗体应答。相比之下,MHC II类敲除小鼠出现较轻的急性心肌炎、持续浸润和强烈纤维化、病毒持续性和弱IgG反应,缺乏病毒中和抗体。结论:免疫缺陷生物在感染CVB3后更容易发生长期心肌损伤。CD4+ T细胞的存在对于预防慢性疾病的发展是必要的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Coxsackievirus B3-induced myocarditis in MHC class II-deficient mice.

Objectives: The pathogenesis of coxsackievirus B3 (CVB3)-induced myocarditis was investigated in immunocompetent C57BL/6 and MHC class II knockout mice with identical genetic backgrounds.

Study design/methods: We analyzed the histology and immunohistology of myocardial injury, the replicating virus titer, and antibody response in the early and late phase of disease.

Results: CVB3-infected C57BL/6 mice showed acute myocarditis, with spontaneous healing, virus elimination, anti-CVB3 IgM/IgG production, and neutralizing antibody response. In contrast, MHC class II knockout mice developed less severe acute myocarditis, persistence of infiltrations and strong fibrosis, virus persistence, and weak IgG response, with absence of virus neutralizing antibodies.

Conclusions: Immunodeficient organisms are more susceptible to long-term heart muscle injuries after infection with CVB3. The presence of CD4+ T cells are necessary to prevent the development of chronic disease.

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