| Project/Area Number |
17500284
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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 |
Laboratory animal science
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| Research Institution | The University of Tokyo |
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Principal Investigator |
SAIJO Shinobu The University of Tokyo, The Institute of Medical Science, Assistant Professor (60396877)
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| Co-Investigator(Kenkyū-buntansha) |
IWAKURA Yoichiro The Institute of Medical Science, Professor (10089120)
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| Project Period (FY) |
2005 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥300,000)
Fiscal Year 2007: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2006: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2005: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Animal disease models / cytokine / Rheumatoid arthritis / Inflammation / Dendritic cells / C-type lectin / Autoimmune / Innate immunity / マウス / 自己免疫疾患 / ノックアウトマウス / トランスジェニックマウス / 発生工学 / 網羅的解析 |
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| Research Abstract |
Recent development of transgenic techniques has made it possible to directly analyze the function of a particular gene in a living animal. These techniques have also made it possible to produce various animal disease models as well as tools to analyze them. In this project, we used two arthritis models that we originally developed. One is HTLV-I Tg mouse and the other one is IL-1Ra KO mouse. To identify genes involving in the pathogenesis of arthritis, we analyzed the gene expression profiles of these animal models by using high-density oligonucleotide arrays. We extracted 554 genes whose expression significantly changed in both models, assuming that pathogenically important genes at the effector phase would change in both models. Interestingly, we found that C-type lectin was up-regulated in the mice. To examine the roles of these genes, we produced three of the C-type lectin KO mice including Dectin-1 and DCIR. In vivo, b-glucan induced cytokine production from wild-type mice and macrophages was abolished in Dectin-1 KO mice. In vivo, Dectin-1 mice was susceptible against fungal infection.
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