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Drug discovery targeting Tet3 for refractory rheumatoid arthritis

Research Project

Project/Area Number 17K09992
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Collagenous pathology/Allergology
Research InstitutionUniversity of Occupational and Environmental Health, Japan

Principal Investigator

Nakano Kazuhisa  産業医科大学, 医学部, 講師 (50406500)

Project Period (FY) 2017-04-01 – 2020-03-31
Project Status Completed (Fiscal Year 2019)
Budget Amount *help
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Keywords関節リウマチ / サイトカイン / 滑膜 / DNAメチル化 / エピゲノム / 滑膜細胞 / エピジェネティクス / 炎症性サイトカイン / TET3 / 糖鎖修飾 / 内科 / 発現制御
Outline of Final Research Achievements

In rheumatoid arthritis (RA), which is a representative autoimmune disease, it is assumed that epigenetic alterations occur in the synovium under the inflammatory environment, resulting in the acquisition of a trait that is more prone to joint destruction and refractory to treatment. In a series of studies, we found that the DNA demethylase TET3 was induced by inflammatory cytokines including TNFα and altered the expression of many genes. As an epigenetic gate-keeper in the pathogenesis of RA, TET3 may play a key role in prolonging inflammation.

Academic Significance and Societal Importance of the Research Achievements

近年、関節リウマチ(RA)においては、生物学的製剤やJAK阻害剤などの分子標的薬の登場により、寛解を目指した治療が可能となったが、分子標的療法でもその3割から4割は治療抵抗性を示し、治療経過とともに難治化する。今回の研究成果は、TET3を標的としたRA滑膜におけるエピゲノム異常の是正が、RA治療のブレークスルーとなりうる可能性を示唆した。

Report

(4 results)
  • 2019 Annual Research Report   Final Research Report ( PDF )
  • 2018 Research-status Report
  • 2017 Research-status Report

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Published: 2017-04-28   Modified: 2021-02-19  

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