| Project/Area Number |
17K09970
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Collagenous pathology/Allergology
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| Research Institution | Chiba University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
廣瀬 晃一 千葉大学, 大学院医学研究院, 特任教授 (90400887)
鈴木 浩太郎 千葉大学, 大学院医学研究院, 准教授 (90554634)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2019: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 関節リウマチ / 自己免疫性関節炎 / 自然リンパ球 / サイトカイン / IL-33 / 脊椎関節炎 / 関節炎 |
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| Outline of Final Research Achievements |
Rheumatoid arthritis (RA) is an autoimmune disease that is characterized by the inflammation of synovial joints. It has been shown that IL-33/ST2 axis or the increase in innate lymphoid cells (ILCs) are involved in the exacerbation of autoimmune diseases. However, the roles of IL-33/ST2 axis and ILCs in the development of autoimmune arthritis such as RA and spondyloarthritis (SpA) remain largely unknown. In this study, we identified the two genes in which expression levels are correlated with disease activity score 28-ESR (DAS28-ESR) and induced in murine ILCs in the presence of IL- 33. We also examined the correlation between the number of ILCs and the ultrasound scores of joints in the patients with RA and SpA. Our data indicate that selective targeting of the IL-33-ST2 axis in ILCs would be a promising strategy in treating autoimmune arthritis.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究により、関節リウマチや脊椎関節炎などの自己免疫性関節炎の発症における自然リンパ球（innate lymphoid cells; ILCs)の役割が明らかになり、自己免疫性関節炎の新規疾患活動性指標、新規治療標的が同定 され、通常治療に抵抗性を示す 自己免疫性関節炎のIL-33/ST2/ILCs軸の制御による新規治療戦略基盤が構築されることが期待される。
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