Periodontal pathology derived from crosstalk between complement and Th17 cells and novel treatment concepts

2023 Fiscal Year Final Research Report

• Project/Area Number: 22K17014
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 57020:Oral pathobiological science-related
• Research Institution: Okayama University
• Principal Investigator: IDEGUCHI Hidetaka 岡山大学, 歯学部, 博士研究員 (80779421)
• Project Period (FY): 2022-04-01 – 2024-03-31
• Keywords: 歯周炎 / 補体 / Th17

Outline of Final Research Achievements

The purpose of this study was to elucidate the details of the mechanism by which the activated complement pathway affects Th17 cell development in periodontitis tissues. Then, we analyzed a series of immunological chain reactions from the activation of the complement pathway to the development of Th17 cells in periodontitis tissue. The results showed that C3, an activated complement degradation product in periodontitis tissue, promotes IL-6 secretion and increases the localization of Th17 cells in the periodontitis tissue by binding to the gingival epithelium in a preferential manner.

Free Research Field

免疫学

Academic Significance and Societal Importance of the Research Achievements

本研究から、歯周病において補体がTh17細胞の分化に及ぼす直接的なメカニズムの一部が明らかになった。これまでに補体とTh17細胞のそれぞれ単独では、様々な学術的背景をもとに歯周病の病態における関与が十分に示されているものの、それぞれの相関について着目した研究はほとんどない。すなわち、本研究の成果は、補体経路を標的とした分子標的薬の歯周治療への臨床応用を円滑に実現する一助となる。さらに、歯周炎のみならず、様々な炎症性免疫疾患の病態を理解するための知見が得られる可能性がある。