| Project/Area Number |
18K19438
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| Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
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| Allocation Type | Multi-year Fund |
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| Review Section |
Medium-sized Section 49:Pathology, infection/immunology, and related fields
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Komatsu Noriko 東京大学, 大学院医学系研究科(医学部), 助教 (20553358)
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| Project Period (FY) |
2018-06-29 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥6,240,000 (Direct Cost: ¥4,800,000、Indirect Cost: ¥1,440,000)
Fiscal Year 2019: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2018: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
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| Keywords | 関節リウマチ / 骨破壊 |
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| Outline of Final Research Achievements |
Rheumatoid arthritis is anautoimmune disease which exhibits chronic inflammation and bone destruction.Osteoclasts are responsible for bone destruction in rheumatoid arthritis,however, osteoclast-inducers have not been identified yet. Here we generated newconditional knockout mice in which osteoclast differentiation factor isspecifically deleted in B cells, T cells and synovial fibroblasts. We foundsynovial fibroblasts are the major osteoclast-inducer cells. It will contributeto the development of new therapies against bone destruction.
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| Academic Significance and Societal Importance of the Research Achievements |
関節リウマチは最も罹患率の高い自己免疫疾患のひとつであるがその病態形成のメカニズムは未だ不明な点が多い。生物学的製剤は全身性の免疫抑制による副作用や効果が認められない症例の存在などの問題を解決するような治療法の開発が喫緊の課題である。本研究より明らかとなった関節リウマチの骨破壊における破骨細胞誘導細胞の決定は長年のRA研究の命題を解決するものでありRA骨破壊のメカニズムの理解のみならず画期的な骨破壊制御法の確立に繋げるうえで学術的にも社会的にも意義があると考えられる。
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