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2022 Fiscal Year Final Research Report

Elucidation of the pathogenic role of microbiota for the development of systemic autoimmune diseases.

Research Project

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Project/Area Number 20K08773
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 54020:Connective tissue disease and allergy-related
Research InstitutionOsaka Metropolitan University (2022)
Osaka City University (2021)
Kyoto University (2020)

Principal Investigator

Hashimoto Motomu  大阪公立大学, 大学院医学研究科, 教授 (60512845)

Project Period (FY) 2020-04-01 – 2023-03-31
Keywords全身性エリテマトーデス / 腸内細菌叢 / Th17細胞 / ZAP70 / TCRシグナル
Outline of Final Research Achievements

In this study, we studied the role of gut microbiome for the development of systemic autoimmune diseases, utilizing an animal model of autoimmunity. SKG mice, which harbor a point mutation in ZAP70 gene, developed SLE or SpA upon B6 or BALB/c genetic background, respectively. The B6-SKG study revealed that 1) Gut microbiome was required for the development of SLE, 2) altered gut microbiome drive Th17 differentiation, 3) Th17 promote systemic autoimmunity via modification of Fc-glycosylation of autoantibodies. The BALB/c-SKG study revealed that 1) Induction of colitis could trigger arthritis in SKG mice, 2) Arthritis was triggered by the translocation of gut microbiome.

Free Research Field

リウマチ学

Academic Significance and Societal Importance of the Research Achievements

SLEやSpAなどの全身性自己免疫疾患の発症メカニズムはまだよくわかっていないが、近年の研究により腸内細菌叢のかかわりが指摘されている。本研究では、腸内細菌叢がSLEやSpAなどの全身性自己免疫疾患の発症につながる分子メカニズムの一端を明らかにした。これらの研究成果は、腸内細菌叢とその生体内移行、もしくはTh17細胞の分化誘導やそれによる自己抗体の糖鎖修飾の変化が、自己免疫疾患の治療ターゲットとなりえることを示した。

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Published: 2024-01-30  

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