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2021 Fiscal Year Final Research Report

Analysis of Inflammatyory Bone Resorption Focused on Immunoreceptor TREM2

Research Project

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Project/Area Number 19K10075
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 57020:Oral pathobiological science-related
Research InstitutionMeikai University

Principal Investigator

BANDOW Kenjiro  明海大学, 歯学部, 講師 (50347093)

Co-Investigator(Kenkyū-buntansha) 長谷川 紘也  明海大学, 歯学部, 講師 (00635899)
Project Period (FY) 2019-04-01 – 2022-03-31
KeywordsTREM2 / LPS / TLR4 / macrophage / M1 polarization / chemokine
Outline of Final Research Achievements

We focused on osteoclast progenitors and macrophages, which are thought to play an important role in diseases that cause inflammatory bone resorption, such as periodontal disease. The purpose of this study is to clarify the role of TREM2, which is commonly present in these cells. TREM2 regulated the expression of chemokines and inflammatory cytokines in macrophages and promoted their polarization to M1 macrophages. Then, it became clear that it is involved in the reception of Caldecrin, which is an osteoclast inhibitory factor. Furthermore, it was found that extracellular TREM2 may have some physiological effect. These results indicate that TREM2 is a key factor in inflammatory bone resorption.

Free Research Field

生化学

Academic Significance and Societal Importance of the Research Achievements

歯周病は歯肉の炎症と歯槽骨の破壊が起きる病気です。炎症と骨吸収の両方に深く関わっているのがマクロファージと破骨細胞です。この2つの細胞は共通の細胞から分化します。我々が注目したのはこの2つの細胞に共通して存在する TREM2 という免疫受容体です。この研究により、TREM2 は炎症を促進する作用と抑制する作用の両方があり、M1 マクロファージと言う炎症性のマクロファージに変化するのを進める作用がある事がわかりました。また、TREM2 の遺伝子をノックアウトした細胞は骨を壊す破骨細胞に変化しませんでした。今後、この TREM2 をターゲットとした歯周病治療法が開発されていく事が期待されます。

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Published: 2023-01-30  

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