| Project/Area Number |
15390154
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Virology
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| Research Institution | HOKKAIDO UNIVERSITY (2004-2005)
Research Institute, Osaka Medical Center for Cancer and Cardiovascular Disaeses (2003) |
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Principal Investigator |
SEYA Tsukasa Hokkaido Univ., Grad.School of Med., Professor, 大学院・医学研究科, 教授 (10301805)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUMOTO Misako Hokkaido Univ., Grad.School of Med., Asso.Professor, 大学院・医学研究科, 助教授 (30332456)
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| Project Period (FY) |
2003 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥13,100,000 (Direct Cost: ¥13,100,000)
Fiscal Year 2005: ¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 2004: ¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 2003: ¥5,500,000 (Direct Cost: ¥5,500,000)
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| Keywords | Measles virus / TLR3 / dendritic cell / dsRNA / CD46 / SLAM / IRE-3 / IFN-β / 麻疹ウィルス / TLR2 / irf-3 |
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| Research Abstract |
TLR3 fosters the induction of type I interferon (IFN) in myeloid dendritic cells (mDCs) in response to exogenously-added dsRNA. Recently, CARD-helicase family proteins, RIG-I and MDA5, are found to be involved in recognition of cytoplasmic dsRNA, presumably of viral origin. Thus, through these sensor molecules virus infection culminates in IFN response. In this study, we have identified the adapter molecule of TLR3 that induces IFN-β and named TICAM-1 (also called Trif). We established CD46/CD150 double TG mice and performed measles infection studies using the TG mice. The TG mice were not measles-sensitive until the IFNAR gene was simultaneously disrupted in addition to the TG. CD11c-positive mDCs were engaged in establishing the initial infection with measles virus. What are the role of TLR3 in mDCs during measles infection and their relation to immune suppression are currently under investigation.
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