SLE小鼠高IgG血症Fcgr2b基因序列分析

Sequence analysis ofFcgr2b gene in hypergammaglo bulinemia model of New Zealand hybrid mice with systemic lupus erythematosis

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 13bp及 3bp。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 .0 0 0 1)。结论 :NZB小鼠Fcgr2b基因启动子区存在碱基缺失 。

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.