New Theory-driven Treatment Development of Polymyositis and Dermatomyositis
| Project/Area Number |
15H04863
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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 |
Collagenous pathology/Allergology
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
KOHSAKA Hitoshi 東京医科歯科大学, 大学院医歯学総合研究科, 教授 (00251554)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥17,550,000 (Direct Cost: ¥13,500,000、Indirect Cost: ¥4,050,000)
Fiscal Year 2017: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2016: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2015: ¥6,630,000 (Direct Cost: ¥5,100,000、Indirect Cost: ¥1,530,000)
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| Keywords | 多発性筋炎 / 皮膚筋炎 / Cタンパク誘導性筋炎 / インターロイキン２３ / 細胞死 / 内科 / 膠原病内科 / リウマチ性疾患 / リンパ球 / I型サイトカイン / II型サイトカイン |
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| Outline of Final Research Achievements |
Based on our Seed and Soil Theory, we conducted some research studies on polymyositis and dermatomyositis (PM / DM) and report here the results of the interleukin (IL) -23 target therapy. As was reported in the patients, serum IL-23 levels were elevated in mice with C protein induced myositis (CIM), a murine model of PM. IL-23p19 was expressed by CD68+ cells in the damaged muscles from the patients. IL-23 were expressed by CD68+ cells in the muscles and draining lymph nodes from CIM mice as well as in chemically injured muscles. Thus, IL-23 production should be associated with the muscle damage. IL-23p19-null mice were resistant to CIM. Administration of anti-IL-23 receptor antibodies ameliorated CIM. When lymph node cells from the CIM mice were transferred into recipients, the myositis was transferred not only to WT but also IL-23p19-null recipients, indicating that IL-23 should activate the autoaggressive T cells. IL-23 should be a promising therapeutic target for PM/DM.
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Report
(4 results)
Research Products
(10 results)
