| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Outline of Final Research Achievements |
In this study, we demonstrated that the level of bcl-2 was significantly increased in tonsil mononuclear cells from the patients with IgA nephropathy compare to control sample. In peripheral mononuclear cells, the level of bcl-2 was also increased, significantly. Since galactose-deficient IgA1 is involved in pathogenesis of IgA nephropathy, our results suggest that bcl-1 might play pivotal role in production of galactose-deficient IgA1. We therefore study the influences of bcl-2 on production of galactose-deficient IgA1. Stimulation of lipopolysaccharide (LPS) or H. Parainfluenzae (HP antigen) on peripheral mononuclear cells induce up-regulation of galactose-deficient IgA1 in supernatant by using ELISA. However, suppression of bcl-2 did not influence the production of galactose-deficient IgA1. Therefore, we could not any correlation between bcl-2 and galactose-deficient IgA1. Further study is required to elucidate the mechanism by which bcl-2 induce IgA nephropathy.
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