SLE小鼠高IgG血症Fcgr2b基因序列分析

目的: 测定系统性红斑狼疮(SLE)小鼠模型-NZB/WF1双亲NZB,NZW小鼠 Fcgr2b基因启动子区核酸序列,明确Fcgr2b基因启动子区的突变性质.方法:扩增NZB,NZW小鼠Fcgr2b基因启动子DNA进行核酸序列分析.采用ELISA法测定、比较(NZB×NZW )F1×NZW回交小鼠Fcgr2b基因B/W型与W/W型组间血清总IgG 水平.结果:NZB小鼠Fcgr2b基因启动子区与正常鼠Balb/C相比存在2个部位碱基缺失,分别为13 bp及3 bp.NZW小鼠除有3个碱基置换外,与Balb/C鼠该基因启动子区序列相同.回交小鼠Fcgr2b基因B/W型组血清总 IgG水平明显高于W/W型组(P<0.0001).结论:NZB小鼠Fcgr2b基因启动子区存在碱基缺失,且该缺失突变可能与血清总IgG水平升高有关.

Sequence analysis of Fcgr2b gene in hypergammaglobulinemia model of New Zealand hybrid mice with systemic lupus erythematosis

Objective: To determine nucleotide sequenc eof susceptibility allele of hypergammaglobulinemia gene, Fcgr2b genes, in system ic lupus erythematosis (SLE) model of New Zealand hybrid mice. Methods:Sequence analysis was used to locate mutation site of Fcgr2b gene, andELISA was used to measure the serum IgG of the group of Fcgr2b gene B/W type an d W/W type. Results: Compared with Balb/C nucleotide sequenceof normal mouse,2 deletion sites were found in Fcgr2b gene promoter region in NZ B mices and changes of 3 base pairs were found in NZW mice. Serum total IgG of t he group of Fcgr2b gene B/W type was obviously higher than that of W/W type (P <0.0001). Conclusion: There were two deletion sites in Fcgr2 b gene promoter region in NZB mice and the deletions could induce hypergammaglob ulinemia.