| Project/Area Number |
18K09561
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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 57020:Oral pathobiological science-related
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| Research Institution | Asahi University |
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Principal Investigator |
Into Takeshi 朝日大学, 歯学部, 教授 (10360918)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 自己免疫性唾液腺炎 / 自然免疫 / シェーグレン症候群 / リンパ球浸潤 / MyD88 / 三次リンパ組織 / 細胞内シグナル伝達 / TLR9 / 樹状細胞 / 疾患モデルマウス |
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| Outline of Final Research Achievements |
In autoimmune sialadenitis (AS), which is found in the autoimmune diseases such as Sjogren's syndrome (SS), salivary secretion is impaired due to destruction of the glandular tissues caused by chronic inflammation accompanied by lymphocyte infiltration, ultimately leading to reduction in the abilities of feeding and oral protection against infections. We found that deletion of the gene of MyD88, which serves as an adapter molecule for the innate immune receptors, in SS model mice resulted in reduction of the frequency of lymphocyte infiltration in salivary glands and salivary gland dysfunction. Our experimental results revealed the pathological role of MyD88 in AS, which are involved in tertiary lymphoid tissue formation, and a series of etiologic candidate genes in AS manifestation.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究では我々が樹立したMyD88欠損SSモデルマウスを用い、種々の分子生物学的実験から、MyD88のASにおける役割、ならびにASの制御において標的となりうる病因的遺伝子群が明らかになった。SSでは関節リウマチや全身性エリテマトーデスなどの自己免疫疾患と比較して免疫抑制薬などによる治療法が確立しておらず、本研究成果から、SSにおける原因療法を基軸とした新しい治療法の確立へと繋がる可能性があり、学術的意義ならびに社会的意義は高いと思われる。
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