| 研究実績の概要 |
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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