2019 Fiscal Year Final Research Report
Identification of molecular mechanisms regulating IFN responses in the novel susceptible gene of Bechet's disease, TRIM39R.
Project/Area Number |
16K21229
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Collagenous pathology/Allergology
Immunology
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Research Institution | Osaka University of Pharmaceutical Sciences (2018-2019) Saga University (2016-2017) |
Principal Investigator |
Kurata Riho 大阪薬科大学, 薬学部, 助教 (70711729)
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Project Period (FY) |
2016-04-01 – 2020-03-31
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Keywords | 自然免疫 / 炎症 / 自己免疫疾患 / ベーチェット病 |
Outline of Final Research Achievements |
Three proteins, TRIM39, TRIM39R, and RPP21, are generated from genes in the susceptible genetic region of Bechet's disease. Among these, only TRIM39R was shown to induce NF-kB and IRF by overexpression. Although TRIM39 and TRIM39R have relative similar three-dimensional structures, but the difference of the C-terminal domain in homodimers was showed by three-dimensional structural analysis. Furthermore, we succeeded in establishing TRIM39R-deficient and human TRIM39R transgenic mice. We are going to continue to analyze molecular mechanism of TRIM39R using various approaches such as, in silico, in vitro and in vivo.
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Free Research Field |
免疫学
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Academic Significance and Societal Importance of the Research Achievements |
本研究において、ベーチェット病(BD)感受性遺伝子として同定したTRIM39Rが炎症性サイトカイン産生およびⅠ型IFN応答を制御することを明らかにした。TRIM39RはBDだけでなく、全身性エリテマトーデスや炎症性腸疾患および乾癬などとの関連も報告されている。また炎症性サイトカイン産生およびⅠ型IFN応答はウイルス感染防御に重要で、TRIM39はウイルス感染後の炎症応答を開始させる重要な分子の1つである可能性が考えられる。今後TRIM39Rの炎症応答における機能解析を進めることで、炎症を伴う様々な感染症や疾患の病態解明に貢献できる。
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