Separation and mapping of multiple genes that control IgE level in Leishmania major infected mice
Separation and mapping of multiple genes that control IgE level in Leishmania major infected mice
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DOI：
10.1038/sj.gene.6363838
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发表时间：
2002-06-01
影响因子：
5
通讯作者：
Lipoldová, M
中科院分区：
文献类型：
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作者：
Badalová, J;Svobodová, M;Lipoldová, M
在感染主要利什曼原虫后，菌株BALB/cHeA（BALB/c）是IgE的高生产者，而STS/A（STS）是IgE的低生产者。我们使用20个重组同源（RC）BALB/c-c-STS/Dem（CcS/Dem）菌株分析了这种菌株差异，这些菌株携带BALB/c背景上菌株STS的12.5%基因的不同随机子集。菌株CcS-16和CcS-20分别表现出高和低IgE水平。在他们的F，杂交BALBIc，我们映射9利什曼原虫主要反应（LMR）位点。我们以前发现其中两种影响CcS-5中的IgE水平。CcS-16中的IgE产生由染色体2、10、16和18上的基因座控制，而CcS-20中的IgE产生由染色体1、3、4、5和8上的基因座控制。第1、4、5、8和10号染色体上的STS等位基因与低IgE产生相关，而第16和18号染色体上的STS等位基因与高IgE产生相关。第2、3号染色体上的基因座没有明显的个体效应，但分别与第10、1号染色体上的基因座互作。染色体10和18上的位点被映射在与人类区域同源的区域中，该区域含有控制血清总IgE和曼氏血吸虫感染强度的基因，这表明一些LMR位点可能参与影响特应性反应和对几种寄生虫的反应的途径。控制抗寄生虫反应的基因的定义将允许更好地了解疾病表型的途径和遗传多样性。
The strain BALB/cHeA (BALB/c) is a high producer, and STS/A (STS) a low producer of IgE after Leishmania major infection. We analyzed this strain difference using 20 recombinant congenic (RC) BALB/c-c-STS/Dem (CcS/Dem) strains that carry different random subsets of 12.5% of genes of the strain STS on the BALB/c background. Strains CcS-16 and -20 exhibit a high and a low IgE level, respectively. In their F, hybrids with BALBIc we mapped nine Leishmania major response (Lmr) loci. Two of them we previously found to influence IgE level in CcS-5. IgE production in CcS-16 is controlled by loci on chromosomes 2, 10, 16 and 18 and in CcS-20 by loci on chromosomes 1, 3, 4, 5 and 8. The STS alleles of loci on chromosomes 1, 4, 5, 8 and 10 were associated with a low, whereas the STS alleles on chromosomes 16 and 18 with a high IgE production. The loci on chromosomes 2 and 3 have no apparent individual effect, but interact with the loci on chromosomes 10 and 1, respectively. The loci on chromosomes 10 and 18 were mapped in the regions homologous with the human regions containing genes that control total serum IgE and intensity of infection by Schistosoma mansoni, suggesting that some Lmr loci may participate in the pathways influencing atopic reactions and responses to several parasites. The definition of genes controlling anti-parasite responses will permit a better understanding of pathways and genetic diversity underlying the disease phenotypes.