| Project/Area Number |
15K19493
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurology
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| Research Institution | Kumamoto University |
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Principal Investigator |
Ikeda Tokunori 熊本大学, 医学部附属病院, 助教 (00613530)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | ES細胞由来ミエロイド細胞 / iPS細胞由来ミエロイド細胞 / 実験的自己免疫性脳脊髄炎 / 免疫抑制性マクロファージ / ES細胞由来ミエロイド細胞 (ES-ML) / iPS細胞由来ミエロイド細胞 (iPS-ML) / 実験的自己免責性脳脊髄炎 (EAE) / 免疫制御 / 細胞治療療法 / 自己免疫疾患 / 自己免疫疾患モデルマウス / EAE |
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| Outline of Final Research Achievements |
I investigated whether or not ES or iPS cell derived myeloid cell (ES-, iPS-ML) had the immunoinhibitory function for experimental autoimmune encephalomyelitis (EAE). The administration of TARIL, which function immuno-inhibitory molecule, gene transferred ES-ML (ES-ML-TRAIL) improved the clinical symptoms of EAE. However, a lot of ES-ML-TRAIL were needed to ameliorate the state of EAE. On the other hand, ES- or iPS-ML functioned like a macrophage, and expressed immunoinhibitory macrophage’s marker, CD163 and CD206. These results suggested the possibility that the application of ES- or iPS-ML was appropriate in the diseases that macrophage’s function were available, but autoimmune diseases.
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