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目的 :定位自发性狼疮小鼠高 Ig G血症遗传易感基因 ,并比较自身与非自身免疫病小鼠间该易感基因是否存在多态性。方法 :建立 (NZB× NZW) F1 × NZW回交小鼠模型 ,采用覆盖小鼠 19条染色体的微卫星多态标记及数量性状位点 (QTL)分析进行基因定位 ,并应用扩增片段长度多态性分析 (Am p FL P)比较该易感基因的多态性。结果 :高 Ig G血症易感基因与小鼠 1号染色体末端微卫星多态标记 Dl Mit36肯定连锁 (L ods值 >3) ,该位点附近存在Fcgr2 b基因 ,且回交小鼠 Fcgr2 b基因 B/ W型组血清总 Ig G水平明显高于 W/ W型组 (P <0 .0 0 0 1) ;自身免疫病NZB小鼠 Fcgr2 b基因启动子区核酸片段长度短于非自身免疫病 NZW、C5 7BL/ 6及 BAL B/ C小鼠。结论 :(NZB×NZW) F1 小鼠高 Ig G血症易感基因为 NZB来源的 Fcgr2 b基因。 NZB小鼠该基因启动子区可能存在碱基缺失
OBJECTIVE: To locate the genetic susceptibility genes of IgA hypergammaglobulinemia in spontaneous lupus mice and to compare the polymorphism of the susceptible genes in mice with non-autoimmune diseases. Methods: The (NZB × NZW) F1 × NZW backcross mouse model was established. Microsatellite markers and quantitative trait loci (QTLs) were used to detect the 19 chromosomes in mice. The amplified fragment length Morphological Analysis (Am p FL P) The susceptibility gene polymorphism was compared. Results: The susceptibility gene of hyperglcaemia was confirmed to be linked with Dl Mit36 microsatellite marker (Lods value> 3) on the chromosome 1 of mouse. The Fcgr2b gene was found near this site, and the Fcgr2b The level of total Ig G in genotype B / W group was significantly higher than that in W / W genotype (P <0.01). The length of nucleic acid fragment in promoter region of Fcgr2 b gene in NZB mice with autoimmune disease was shorter than that in non-autoimmunity NZW, C5 7BL / 6, and BAL B / C mice. CONCLUSIONS: The (NZB × NZW) F1 mouse hyperglioemia susceptibility gene is the NZB-derived Fcgr2 b gene. NZB mouse gene promoter region may exist base deletion