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

被引:64
|
作者
Terajima, Masanori [1 ]
Hayasaka, Daisuke [1 ]
Maeda, Ken [1 ]
Ennis, Francis A. [1 ]
机构
[1] Univ Massachusetts, Sch Med, Ctr Infect Dis & Vaccine Res, Worcester, MA 01655 USA
关键词
hantavirus; endothelial cells; cytotoxic T lymphocytes; PD-1; PD-L1; PD-L2; hantavirus pulmonary syndrome; hemorrhagic fever with renal syndrome;
D O I
10.1016/j.imlet.2007.08.003
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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 vir-us, 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. (C) 2007 Elsevier B.V. All rights reserved.
引用
收藏
页码:117 / 120
页数:4
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