Immune-Mediated Pathogenesis of Borna Disease

R. Rott , S. Herzog, J. Richt, L. Stitz
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引用次数: 29

Abstract

Borna disease is an endemic progressive encephalomyelitis of horses and sheep prevalent in central Europe. A wide variety of animal species, ranging from chickens to primates can be infected experimentally with the causative virus, which is only poorly characterized. Furthermore, BD virus-specific antibodies have been detected in sera and cerebrospinal fluids of psychiatric patients.

Our studies on the pathogenesis of BD have shown that — at least in rats — the disease is not caused by the infecting virus itself, but by a virus-induced immunopathological reaction. Thus, after intracerebral infection immunoincompetent rats do not get the disease despite persistent virus replication in cells of the central nervous system. However, after adoptive transfer of immune cells from diseased rats, immunoincompetent rats exhibit full-blown BD. Recently, we have been successful in establishing a virus-specific T cell line of the helper/inducer phenotype (CD4+). This T cell was shown to play an important role in the pathogenesis of BD, suggesting that the disease is caused by a delayed type hypersensitivity reaction.

博纳病的免疫介导发病机制
博纳病是一种在中欧流行的马和羊的地方性进行性脑脊髓炎。从鸡到灵长类动物,各种各样的动物物种都可以通过实验感染这种致病病毒,但目前对这种病毒的特征知之甚少。此外,在精神病患者的血清和脑脊液中检测到BD病毒特异性抗体。我们对BD发病机制的研究表明,至少在大鼠中,这种疾病不是由感染病毒本身引起的,而是由病毒诱导的免疫病理反应引起的。因此,在脑内感染后,尽管病毒在中枢神经系统细胞中持续复制,但免疫功能低下的大鼠不会患病。然而,在将患病大鼠的免疫细胞过继移植后,免疫功能不全的大鼠表现出全面的BD。最近,我们已经成功地建立了一种辅助/诱导表型(CD4+)的病毒特异性T细胞系。该T细胞在BD的发病机制中发挥了重要作用,提示该疾病是由延迟型超敏反应引起的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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