| Project/Area Number |
16590834
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | Nagasaki University |
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Principal Investigator |
NAKAMURA Tatsufumi Nagasaki Univ., Grad.Sch.of BioM.Sci, Associate Professor, 大学院・医歯薬学総合研究科, 助教授 (00198219)
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| Co-Investigator(Kenkyū-buntansha) |
EGUCHI Katsumi Nagasaki Univ., Grad.Sch.of BioM.Sci, Professor, 大学院・医歯薬学総合研究科, 教授 (30128160)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2005: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2004: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | HAM / HTLV-I / Th1 / IFN-γ / p38MAPK signaling / IL-2 / IL-2R signaling / IL-2R / p38 MAPK / HTLV-I p19 |
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| Research Abstract |
Th1 activation based on high HTLV-I proviral load plays an important role in the development of HTLV-I-associated myelopathy (HAM). In order to elucidate the cell signaling pathway involved in this situation, we analyzed the relationship between the expression of IFN-γ and HTLV-I and IL-2 receptor (IL-2R)/p38 MAPK signaling. At first, we demonstrated that activation of p38 MAPK signaling is involved in this situation. Secondly, the importance of IL-2/IL-2R signaling located in the upstream of p38 MAPK was suggested for IFN-γ and HTLV-I expression. Overall, our results indicate that IL-2R/p38 MAPK signaling pathway may be a potential target in therapeutic strategies for HAM.
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