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目的 :定位自发性SLE模型——— (NZB×NZW)F1 小鼠高IgG血症的遗传易感基因。方法 :建立 (NZB×NZW )F1 ×NZW回交小鼠模型 ,采用覆盖小鼠 19条染色体的多态性微卫星遗传标记及数量性状位点 (QTL)分析进行基因定位。结果 :高IgG血症易感基因与小鼠第 1条染色体末端 92 .3cM处微卫星遗传标记D1Mit36肯定连锁 (Lods值 >3) ,该位点附近 92 .0cM处存在Fcgr2b基因 ,且回交小鼠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×NZW)F1 小鼠高IgG血症易感基因为NZB来源的Fcgr2b基因
PURPOSE: To locate the genetic predisposition genes of hyperglycemia in mice with spontaneous SLE model --- (NZB × NZW) F1. Methods: A (NZB × NZW) F1 × NZW backcross mouse model was established. The genetic loci were detected by using genetic markers and quantitative trait loci (QTL) of 19 microsatellite markers covering mice. RESULTS: The hypergammaglobulinemia susceptibility gene was positively linked to the microsatellite marker D1Mit36 at 92.3cM at chromosome 1 end of mouse (Lods value> 3). The Fcgr2b gene was located at 92 .0cM near the site and was backcrossed The total serum IgG level of mouse Fcgr2b BW group was significantly higher than that of WW group (P <0.01). CONCLUSIONS: The hypergammaglulonemia susceptibility gene in (NZB × NZW) F1 mice is the NZB-derived Fcgr2b gene