Ｂリンパ球の分化と自己免疫に関するマウスｇｐ４９Ｂの機能解析
| Project/Area Number |
16J01922
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| Research Category |
Grant-in-Aid for JSPS Fellows
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| Allocation Type | Single-year Grants |
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| Section | 国内 |
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| Research Field |
Immunology
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| Research Institution | Tohoku University |
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Principal Investigator |
WONG YI LI 東北大学, 生命科学研究科, 特別研究員(DC1)
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| Project Period (FY) |
2016-04-22 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 2018: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2017: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2016: ¥700,000 (Direct Cost: ¥700,000)
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| Keywords | glycoprotein 49B / SLE / plasma cell / autoimmunity / pathogenic antibody / gp49B |
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| Outline of Annual Research Achievements |
gp49b deficiency in BXSB/Yaa mice reduced serum titer of anti-dsDNA IgG and prolonged survival rate with mild kidney inflammation. gp49B-deficient BXSB/Yaa mice have regained marginal zone B cells and slight reduction of monocytosis. These observations suggested a pathogenic role of gp49B in SLE disease.
BXSB/Yaa mice treated with anti-gp49 monoclonal antibody showed suppression of increase in serum titer of anti-dsDNA IgG, without any cells depletion (including number of pathogenic cells).
gp49B deficiency in aged FcgammaRIIB-knockout SLAM129(RIIB-/-) female mice showed heightened autoimmunity, with lesser longevity and more switched memory B cells. The difference between BXSB/Yaa and RIIB-/- mice could be the amplification effect of gp49B deficiency to tolerance loss from RIIB deficiency.
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| Research Progress Status |
平成30年度が最終年度であるため、記入しない。
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| Strategy for Future Research Activity |
平成30年度が最終年度であるため、記入しない。
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Report
(3 results)
Research Products
(5 results)
