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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 ,且该缺失突变可能与血清总IgG水平升高有关
OBJECTIVE: To determine the promoter region of Fcgr2b gene in NZB and NZW mice of SLE mouse model NZB / WF1 and to determine the mutation of Fcgr2b promoter region. Methods: The promoter DNA of Fcgr2b gene of NZB and NZW mice was amplified for nucleic acid sequence analysis. ELISA method was used to determine the total serum IgG levels between B / W and W / W groups of Fcgr2b gene in (NZB × NZW) F1 × NZW backcross mice. Results: There were two base deletions in the promoter region of Fcgr2b gene in NZB mice compared with Balb / C mice, which were 13bp and 3bp, respectively. The NZW mouse has the same sequence as the promoter region of Balb / C mouse except 3 base substitutions. The total serum IgG level of Fcgr2b gene B / W group in backcross mice was significantly higher than that in W / W group (P <0.01). CONCLUSION: There is a base deletion in the promoter region of Fcgr2b gene in NZB mice, and this deletion mutation may be related to the increase of serum total IgG level