| Project/Area Number |
17H06653
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
General internal medicine(including psychosomatic medicine)
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
UMEZAWA Natsuka 東京医科歯科大学, 医学部附属病院, 助教 (90801530)
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| Project Period (FY) |
2017-08-25 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 多発性筋炎 / 皮膚筋炎 / マクロファージ / 骨格筋 / トランスレーショナルリサーチ / 免疫学 / 炎症性筋疾患 |
|---|
| Outline of Final Research Achievements |
We previously found that the macrophages in inflamed muscles from mice with experimental myositis exacerbated myositis through the production of IL-23. In this study, we focused on the precise role of macrophages in idiopathic inflammatory myopathies (IIMs) other than IL-23 production. The techniques to obtain the macrophages in the muscles from patients with IIMs were established for the first time in this study. However, the number of the obtained macrophages was insufficient to separate to subsets or to analyse the molecular expression. In the future experiments, we analysis the limited number of macrophages with single cell RNA-seq. In addition, we obtained mice with human diphtheria toxin receptor to deplete the macrophages. Induction of experimental myositis in the mice would help understanding on the roles of macrophages in IIM.
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| Academic Significance and Societal Importance of the Research Achievements |
従来のT細胞を標的とした治療法に加え、本研究で目的とするマクロファージを標的とした治療を開発することで、治療抵抗性の患者や、副腎皮質ステロイドをはじめとした従来の治療に不耐用であった患者の治療に貢献できる。また、従来筋組織は固定標本の免疫組織学的染色にとどまったが、本研究で確立した手法を用いることにより、筋組織から生細胞を採取することで、生体内での機能をより反映した解析を行うことが可能となった。
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