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Studies on the induction of pathogenic T cell by endoplasmic reticulum stress and the pathogenesis of systemic lupus erythematosus

Research Project

Project/Area Number 18K06933
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 48040:Medical biochemistry-related
Research Institution株式会社膠原病研究所

Principal Investigator

Tsumiyama Ken  株式会社膠原病研究所, 研究部, 主任研究員 (20514607)

Project Period (FY) 2018-04-01 – 2021-03-31
Project Status Completed (Fiscal Year 2020)
Budget Amount *help
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2019: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Keywords全身性エリテマトーデス(SLE) / 小胞体ストレス / CD4 T細胞 / 全身性エリテマトーデス
Outline of Final Research Achievements

We examined the involvement of endoplasmic reticulum (ER) stress in the induction of pathogenic T cell that causes systemic lupus erythematosus (SLE). We found that when SLE was induced in mice, the expression of unfolded protein response (UPR)-related molecules was increased in CD4 T cells. In these CD4 T cells, the gene expression of several molecules related to Wnt signaling pathway was changed. In vivo administration of ER stress inducer accelerated the production of autoantibody and autoimmune tissue injury. The result suggests that ER stress contributes to the pathogenesis of SLE by modulating the function of T cell.

Academic Significance and Societal Importance of the Research Achievements

本研究により、難病であるSLEの発症機序の一端を明らかにすることができた。この中で、細胞の恒常性を維持する機構である小胞体ストレス応答がT細胞の変調を引き起こし、SLEの病態形成に関与することを示した。これにより、小胞体ストレス応答関連分子を標的としたSLEの治療の可能性を示すことができたと考える。

Report

(4 results)
  • 2020 Annual Research Report   Final Research Report ( PDF )
  • 2019 Research-status Report
  • 2018 Research-status Report
  • Research Products

    (3 results)

All 2019

All Presentation (3 results) (of which Int'l Joint Research: 1 results)

  • [Presentation] SLEの発症を誘導する自己抗体産生誘導性CD4 T細胞(aiCD4 T細胞)の解析;濾胞性ヘルパーT細胞とIL-21産生CXCR5-ICOShiPD-1hi CD4 T細胞2019

    • Author(s)
      積山賢、塩沢俊一
    • Organizer
      第63回日本リウマチ学会総会・学術集会
    • Related Report
      2019 Research-status Report
  • [Presentation] SLE発症の自己臨界点説(SLEが自己臨界点を超える繰り返す抗原刺激の結果発症する)の証明:DOCK8陽性CD4 T細胞=aiCD4 T細胞によるSLEの発症2019

    • Author(s)
      塩沢俊一、積山賢、櫻井恵一、香川英俊、山根隆志、織部元廣、石井宏治、堀内孝彦、吉原良祐、村田美紀、塩沢和子
    • Organizer
      第63回日本リウマチ学会総会・学術集会
    • Related Report
      2019 Research-status Report
  • [Presentation] Systemic lupus erythematosus (SLE) is caused by expanded DOCK8-positive autoantibody-inducing CD4 T (aiCD4 T) cell2019

    • Author(s)
      Shiozawa S, Tsumiyama K, Miyazaki Y, Sakurai K, Horiuchi T, Oribe M, Yamane T, Kagawa H, Shiozawa K
    • Organizer
      アメリカリウマチ学会2019
    • Related Report
      2019 Research-status Report
    • Int'l Joint Research

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Published: 2018-04-23   Modified: 2022-01-27  

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