| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Outline of Final Research Achievements |
I have reported that CD8-positive T cells are related to the pathogenesis of hemorrhagic fever with renal syndrome by using a mouse model. In this study, I tried to elucidate the mechanism by which CD8-positive T cells cause disease by using closely related high and low pathogenic clones. The quantity of hantavirus-specific T lymphocytes (CTLs) in high pathogenic clone-infected mice was comparable to that in low-pathgenic clone-infected mice. However, high pathogenic clone-infected mice showed up-regulation of genes relating to the effector function and chemotaxis of CTLs as well as genes relating to the activation-induced cell death of T cells, suggesting higher activity of CTLs in high pathogenic clone-infected mice. Considering the efficient viral growth of high pathogenic clone in kidney, the balance between quantities of the target and effector would be also important for disease outcome.
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