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

BXSB/YAA小鼠gp49b缺乏可降低血清抗dsDNA免疫球蛋白滴度，延长存活率，并伴有轻度肾脏炎症。Gp49B基因缺陷的BXSB/YAA小鼠恢复了边缘带B细胞，单核细胞数略有减少。这些观察表明gp49B在SLE疾病中起致病作用。经抗gp49单抗处理的BXSB/Yaa小鼠表现出抑制血清抗dsDNA抗体滴度的增加，而没有任何细胞耗竭(包括致病细胞数量)。在老年FcGammaRIIB基因敲除SLAM129(RIIB-/-)雌性小鼠中，gp49B缺乏表现出较高的自身免疫力，寿命较短，切换记忆B细胞较多。BXSB/YaA和RIIB-/-小鼠之间的差异可能是gp49B缺陷对RIIB缺陷所致的耐受性丧失的放大作用。

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.