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首页> 外文期刊>Archives of virology >Involvement of CD8(+) T cells in the development of renal hemorrhage in a mouse model of hemorrhagic fever with renal syndrome
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Involvement of CD8(+) T cells in the development of renal hemorrhage in a mouse model of hemorrhagic fever with renal syndrome

机译：CD8（+）T细胞参与肾综合征出血发热小鼠肾脏出血的发展

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Hemorrhagic fever with renal syndrome (HFRS) is caused by hantavirus infection. Although host immunity is thought to be involved in the pathogenesis of HFRS, the mechanism remains to be elucidated. A mouse model of HFRS, which showed renal hemorrhage similar to that seen in patients, has been developed previously. In this study, we aimed to clarify whether CD4(+) and CD8(+) T cells are involved in the development of renal hemorrhage in the mouse model. At 2 days before virus inoculation, CD4(+) or CD8(+) T cells in 6-week-old BALB/c mice were depleted by administration of antibodies. The CD4(+) T cell-depleted mice developed signs of disease such as transient weight loss, ruffled fur and renal hemorrhage as in non-depleted mice. In contrast, the CD8(+) T cell-depleted mice showed no signs of disease. After determination of CTL epitopes on the viral glycoprotein in BALB/c mice, the quantity of virus-specific CTLs was analyzed using an MHC tetramer. The quantity of virus-specific CTLs markedly increased in spleens and kidneys of virus-infected mice. However, the quantity in high-pathogenic clone-infected mice was comparable to that in low-pathogenic clone-infected mice. We previously reported that the high-pathogenic clone propagated more efficiently than the low-pathogenic clone in kidneys of mice during the course of infection. Therefore, there is a possibility that the balance between quantities of the target and effector is important for disease outcome. In conclusion, this study showed that CD8(+) T cells are involved in the development of renal hemorrhage in a mouse model of HFRS.
机译：患有肾综合征（HFR）的出血热是由Hantavirus感染引起的。虽然宿主抗扰度被认为参与HFR的发病机制，但该机制仍有待阐明。先前已经开发出类似于患者中所见的肾脏出血的HFR的小鼠模型。在这项研究中，我们旨在阐明CD4（+）和CD8（+）T细胞是否参与小鼠模型中肾脏出血的发育。在病毒接种前2天，通过施用抗体耗尽6周龄BALB / C小鼠中的CD4（+）或CD8（+）T细胞。 CD4（+）T细胞耗尽的小鼠发育了疾病的迹象，如在非耗尽的小鼠中的瞬态减肥，荷叶边和肾脏出血。相反，CD8（+）T细胞耗尽的小鼠显示出疾病的迹象。在BALB / C小鼠中测定病毒糖蛋白上的CTL表位后，使用MHC四聚体分析病毒特异性CTL的量。病毒特异性CTL的数量显着增加了病毒感染小鼠的脾脏和肾脏。然而，高病原克隆感染的小鼠中的量与低致病克隆感染的小鼠相当。我们之前报道，在感染过程中，高病原克隆比小鼠肾脏中的低致病克隆更有效地繁殖。因此，存在靶和效应器之间的平衡可能对疾病结果很重要。总之，该研究表明，CD8（+）T细胞参与HFR小鼠模型中肾出血的发育。

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