Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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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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