Pathogenesis elucidation of seronegative spondyloarthritis using patient-derived iPSCs

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K15663
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Orthopaedic surgery
• Research Institution: Kyoto University
• Principal Investigator: Yoshitomi Hiroyuki 京都大学, ウイルス・再生医科学研究所, 准教授 (50402920)
• 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)
• 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)
• Project Period (FY): 2016-04-01 – 2018-03-31
• 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

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.

Free Research Field

リウマチ学、遺伝子編集