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2020 Fiscal Year Final Research Report

Analysis of pathogenesis of oral lichen planus -Cytokine network connecting dendritic cells and T cells-

Research Project

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Project/Area Number 17K11846
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Surgical dentistry
Research InstitutionKyushu University

Principal Investigator

Hayashida Junnosuke  九州大学, 歯学研究院, 共同研究員 (80432920)

Co-Investigator(Kenkyū-buntansha) 中村 誠司  九州大学, 歯学研究院, 教授 (60189040)
Project Period (FY) 2017-04-01 – 2021-03-31
KeywordsカテプシンK / pDC / mDC / 自己免疫性炎症 / Th17
Outline of Final Research Achievements

For the purpose of identifying epithelial-derived disease-related molecules involved in the pathogenesis of oral lichen plan (OLP), pathological sections of patients were comprehensively analyzed by DNA microarray. As a result, cathepsin K (CTSK) was extracted as a humoral factor involved in the activation of Th (helper T) cells. CTSK was strongly expressed in the epithelium of the lesion and the infiltration of inflammatory cells immediately below it. Dendritic cells were extracted from human peripheral blood and stimulated with CTSK. As a result, it was suggested that dendritic cells such as mDC and pDC play an important role in the activation of Th subset of OLP.

Free Research Field

口腔粘膜疾患における免疫

Academic Significance and Societal Importance of the Research Achievements

WHOはOLPをpremalignant conditionからpotentially malignant disorderと位置づけたが、実際一部のOLP症例では扁平上皮癌への悪性転化が認められるため、OLPの病態進展をいかに抑制するかが治療上重要と考えられた。今回の研究によってカテプシンKがIL-6やIL-23などの炎症性サイトカイン産生を制御することが示唆され、Th17細胞分化を誘導することで自己免疫性炎症を引き起こすことが示唆された。これらの細胞に関与するDCサブセットをさらに明らかにすることで疾患の発症や重症化のメカニズム解明および新規治療薬の開発が期待される。

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Published: 2022-01-27  

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