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博尔纳病的免疫介导发病机制。

Immune-mediated pathogenesis of Borna disease.

作者信息

Rott R, Herzog S, Richt J, Stitz L

机构信息

Institut für Virologie, Justus-Liebig-Universität Giessen.

出版信息

Zentralbl Bakteriol Mikrobiol Hyg A. 1988 Nov;270(1-2):295-301. doi: 10.1016/s0176-6724(88)80166-4.

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.

摘要

博尔纳病是中欧地区马和羊中流行的一种地方性进行性脑脊髓炎。从鸡到灵长类等多种动物都可通过实验感染致病病毒,而该病毒的特征了解甚少。此外,在精神病患者的血清和脑脊液中检测到了博尔纳病病毒特异性抗体。我们对博尔纳病发病机制的研究表明,至少在大鼠中,该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所致。因此,脑内感染后,免疫缺陷大鼠尽管病毒在中枢神经系统细胞中持续复制,但并未发病。然而,将患病大鼠的免疫细胞过继转移后,免疫缺陷大鼠会出现典型的博尔纳病症状。最近,我们成功建立了具有辅助/诱导表型(CD4+)的病毒特异性T细胞系。该T细胞在博尔纳病发病机制中起重要作用,提示该病是由迟发型超敏反应引起的。

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