| Project/Area Number |
11671058
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Tokyo Women's Medical University, (TWMU) |
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Principal Investigator |
NITTA Kosakn Tokyo Women's Medical University, Dept. of Med. Assistant Prof., 医学部, 講師 (50241071)
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| Co-Investigator(Kenkyū-buntansha) |
UCHIDA Keiko Tokyo Women's Medical University, Dept. of Med. Lecturer, 医学部, 助手 (60246478)
KAWASHIMA Akira Tokyo Women's Medical University, Dept. of Med. Assistant Prof., 医学部, 講師 (20224769)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 2000: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1999: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | CD28 / CTLA-4 / Costimulation / Glomernlonephritis / Mice / T-cells / 抗糸球体基底膜抗体 / 免疫複合体型糸球体腎炎 / 半月体 / 補助シグナル / B細胞 |
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| Research Abstract |
Engagement of CD28 on T cells provides an essential costimulatory signal for T cell activation and differentiation. The current studies were designed to examine the role of CD28 in the pathogenesis of immune-complex glomerulonephritis (GN). Induction of anti-GBM experimental GN was completely prevented in CD28-deficient (KO) mice. In addition, CD28KO mice showed no increase in serum ds-DNA titers and no deposition of IgG in the GBM.These results suggest that effective inhibition of CD28-dependent autoantibody production could be useful in the treatment for antibody-dependent GN.We then investigated the effect of soluble form CTLA-4 on spontaneous IgA nephropathy in ddY mice. Mice trcated with CTLA4Ig showed a significant reduction in proteinuria and mesangioproliferative glomerulonephritis, inplicating that a costimulatory signal via CD28/B7 may play a crucial role in thc development of IgA nephropathy. Further studies are required to find more effective clue to inhibit CD28/B7 costimulatory stignal.
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