2023 Fiscal Year Final Research Report
Elucidation of the pathogenic mechanism of IgA nephropathy by MHC class II gene polymorphisms
| Project/Area Number |
21K08286
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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 53040:Nephrology-related
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| Research Institution | Juntendo University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
鈴木 仁 順天堂大学, 医学部, 教授 (10468572)
鈴木 祐介 順天堂大学, 大学院医学研究科, 教授 (70372935)
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| Project Period (FY) |
2021-04-01 – 2024-03-31
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| Keywords | IgA腎症 / MHC classⅡ / 糖鎖異常IgA / IgA型自己抗体 |
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| Outline of Final Research Achievements |
To clarify the involvement of MHC class II gene polymorphisms in the pathogenesis of IgA nephropathy (IgAN), we used ddY mice, a spontaneous model of IgAN. DdY mice can be divided into three categories according to MHC class II haplotypes. Phenotypic differences between haplotypes were evaluated, however, no differences in IgA deposition on glomeruli or phenotype were observed. In addition, although galactose-deficient IgA and autoantibodies against renal mesangial proteins, which have been suggested to be pathogenic in IgAN, were also examined, there are question whether galactose-deficient IgA or autoantibodies were pathogenic in IgAN could not be identified. Thus, we were unable to determine the association of MHC class II with the development of IgAN in this study.
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| Free Research Field |
腎臓
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| Academic Significance and Societal Importance of the Research Achievements |
ゲノムワイド関連解析により、IgA腎症におけるMHC classⅡ遺伝子変異と病態の関与が示唆されている。ddYマウスのMHC classⅡのハプロタイプが３つに分類できること、さらにddYマウスの発症様式が週齢に応じて３つに分類できることから、病態とMHC classⅡに着目して検討をおこなった。本研究ではこれらの関連を明らかにすることはできなかったが、IgA腎症の動物モデルを用いて検証した研究というのは皆無あり、今後のIgA腎症のMHC classⅡの遺伝子多型による研究において新たな知見を与えうると考える。
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