2021 Fiscal Year Final Research Report
Functional analysis of transcription factor MafB in autoimmune diseases
| Project/Area Number |
19K07482
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 49030:Experimental pathology-related
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| Research Institution | Kagawa University |
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Principal Investigator |
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| Project Period (FY) |
2019-04-01 – 2022-03-31
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| Keywords | 自然免疫 / 形質細胞様樹状細胞 / 転写因子MafB / 免疫抑制 |
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| Outline of Final Research Achievements |
Interferon (IFN) over-secreted from plasmacytoid dendritic cells (pDCs) cause to the pathogenesis of the autoimmune disease psoriasis vulgaris. However, the mechanism of negative regulation of IFN by pDCs remains unknown. In vivo studies indicated that MafB is involved in resistance against imiquimod-induced psoriasis-like skin inflammation. These findings demonstrate that MafB acts as a negative regulator of IFN induction in pDCs and plays an important role in maintaining immune homeostasis.
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| Free Research Field |
自然免疫
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| Academic Significance and Societal Importance of the Research Achievements |
乾癬における病態形成には、形質細胞様樹状細胞（pDC）の存在とインターフェロン（IFN）が極めて重要な因子であることが示唆されていたが、疾患の根本的な発症や病態形成メカニズムは不明であった。本研究において、pDCのIFN産生を抑制するシステムという、より根源的な部分が明らかになったことで、疾患の詳細な病態メカニズムの解明と根本的な治療法開発に大きく飛躍することが期待される。
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