2014 Fiscal Year Final Research Report
Pathogenic role of galactose-deficient IgA1 contained immune complexes and tonsillar cells in IgA nephropathy
| Project/Area Number |
24591213
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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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| Research Field |
Kidney internal medicine
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| Research Institution | Juntendo University |
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Principal Investigator |
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| Research Collaborator |
SUZUKI Yusuke 順天堂大学, 医学部, 准教授
YANAGAWA Hiroyuki 順天堂大学, 医学部
SASAKI Yohei 順天堂大学, 医学部
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Keywords | IgA腎症 / 糖鎖 / 免疫複合体 / 粘膜免疫 / 扁桃 |
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| Outline of Final Research Achievements |
Galactose-deficient IgA1 (Gd-IgA1) and Gd-IgA1-specific autoantibodies have a crucial roles in the pathogenesis of IgA nephropathy (IgAN). Inflammatory cytokine, such as IL-6 and IL-4, could increase the production of Gd-IgA1 in IgA1-producing cell lines through complex changes of specific glycosyltransferases. Tonsillectomy plus corticosteroid therapy (TSP) is one of the effective therapies for IgAN. After TSP, serum levels of Gd-IgA1 and Gd-IgA1-specific autoantibodies significantly decreased. Thus, a part of Gd-IgA1 and Gd-IgA1-specific autoantibodies in circulation might be originated from palatine tonsil. Dysregulation of mucosal immunity may induce the overproduction of Gd-IgA1 and Gd-IgA1-specific autoantibodies via activation of TLR9 and APRIL.
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| Free Research Field |
IgA腎症
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