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汉坦病毒肺综合征和肾综合征出血热的免疫发病机制:CD8 + T细胞会引发病毒性出血热中的毛细血管渗漏吗?

Immunopathogenesis of hantavirus pulmonary syndrome and hemorrhagic fever with renal syndrome: Do CD8+ T cells trigger capillary leakage in viral hemorrhagic fevers?

作者信息

Terajima Masanori, Hayasaka Daisuke, Maeda Ken, Ennis Francis A

出版信息

Immunol Lett. 2007 Nov 15;113(2):117-20. doi: 10.1016/j.imlet.2007.08.003. Epub 2007 Sep 12.

Abstract

There are many viruses known to cause viral hemorrhagic fevers in humans. The mechanisms causing hemorrhage are likely to vary among viruses. Some viruses, such as Marburg virus, are directly cytopathic to infected endothelial cells, suggesting infection of endothelial cells alone can cause hemorrhage. On the other hand, there are viruses which infect endothelial cells without causing any cytopathic effects, suggesting the involvement of host immune responses in developing hemorrhage. Typical examples of these include viruses of the hantavirus species. We hypothesize that impairment of endothelial cell's defense mechanisms against cytotoxic CD8+ T cells is the mechanism of capillary leakage in hantavirus pulmonary syndrome and hemorrhagic fever with renal syndrome, which may be common to other viral hemorrhagic fevers. CD8+ T cells may be a potential target for therapy of some viral hemorrhagic fevers.

摘要

已知有许多病毒可导致人类病毒性出血热。不同病毒引起出血的机制可能有所不同。一些病毒,如马尔堡病毒,对受感染的内皮细胞具有直接细胞病变作用,这表明仅内皮细胞感染就可导致出血。另一方面,有些病毒感染内皮细胞却不产生任何细胞病变效应,这表明宿主免疫反应参与了出血的发生。这类病毒的典型例子包括汉坦病毒属的病毒。我们推测,内皮细胞针对细胞毒性CD8 + T细胞的防御机制受损是汉坦病毒肺综合征和肾综合征出血热中毛细血管渗漏的机制,这可能也是其他病毒性出血热的共同机制。CD8 + T细胞可能是某些病毒性出血热治疗的潜在靶点。

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