Pathogenesis elucidation of seronegative spondyloarthritis using patient-derived iPSCs
| Project/Area Number |
16K15663
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Kyoto University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
戸口田 淳也 京都大学, ウイルス・再生医科学研究所, 教授 (40273502)
金 永輝 京都大学, 医学研究科, 特定助教 (90620344)
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| Co-Investigator(Renkei-kenkyūsha) |
KAWAMOTO Hiroshi 京都大学, ウイルス・再生医科学研究所, 教授 (00343228)
MASUDA Kyoko 京都大学, ウイルス・再生医科学研究所, 助教 (40565777)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | iPS細胞 / 血清反応陰性脊椎関節炎 / HLA B27 / 遺伝子編集 / CRISPR-Cas9 / CXCL13 / 血清反応陰性関節炎 / 強直性脊椎炎 / ゲノム編集 |
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| Outline of Final Research Achievements |
During this project, we established iPSCs from three patients with ankylosing spondylitis, a seronegative spondyloarthritis. To address pathogenic function of HLA B27, we also successfully established HLA B27 deficient iPSCs from two patients using CRISPR/Cas9 genome-editing. Furthermore, we investigated the role of T cells in human chronic inflammatory diseases, because HLA is most contributing factor to human autoimmune arthritis; and showed that in synovium of rheumatoid arthritis a contrast disease of seronegative spondyloarthritis, transcription factor Sox4 contributes to the pathogenesis of chronic inflammation by CXCL13 production from CD4+ T cells.
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Report
(4 results)
Research Products
(7 results)
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[Journal Article] Human Sox4 facilitates the development of CXCL13-producing helper T cells in inflammatory environments.2018
Author(s)
Yoshitomi H, Kobayashi S, Miyagawa-Hayashino A, Okahata A, Doi K, Nishitani K, Murata K, Ito H, Tsuruyama T, Haga H, Matsuda S, Toguchida J
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Journal Title
Nature Communications
Volume: 9
Issue: 1
Pages: 3762-3762
DOI
NAID
Related Report
Peer Reviewed / Open Access
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