Genomics of vasculitis: lessons from mouse models.
Genomics of vasculitis: lessons from mouse models.
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DOI：
10.3400/avd.oa.12.00096
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发表时间：
2013-01-01
影响因子：
0.8
通讯作者：
Mori, Shiro
中科院分区：
文献类型：
--
作者：
Nose, Masato;Komori, Hiroaki;Mori, Shiro
对小鼠模型的基因组分析可能有助于阐明系统性血管炎复杂的临床病理学表现。在MRL小鼠模型血管炎易感基因位点的研究中，我们发现系统性血管炎是通过多个基因位点的累积效应发展的，每个基因位点本身在诱导相关表型方面没有显著作用，因此表明是多基因系统。小鼠以叠加方式发生血管炎，具有分层效应。某些易感位点似乎与其他胶原性疾病的易感位点相同。此外，控制血管炎的组织特异性的位点存在。血管炎的一个位置候选基因在编码区显示等位基因多态性，因此可能导致其功能的质的差异。因此，具有这种等位基因多态性的多基因的特定组合可能因此在导致级联反应发展为血管炎以及系统性血管炎的规律变化中起关键作用。这被称为系统性血管炎的多基因网络。（J Jpn科尔血管学杂志，2009，49：11-16）。
A genome analysis of mouse models may shed some light on the complex clinicopathological manifestations of systemic vasculitis. In the study of susceptibility loci to vasculitis in MRL mouse models, we found that systemic vasculitis developed through the cumulative effect of multiple gene loci, each of which by itself did not have a significant effect in inducing the related phenotype, thus indicating a polygenic system. The mice developed vasculitis in an additive manner with a hierarchical effect. Some of the susceptibility loci seemed to be common to those in other collagen diseases. Moreover, the loci controlling tissue specificity of vasculitis were present. One of the positional candidate genes for vasculitis showed an allelic polymorphism in the coding region, thus possibly causing a qualitative difference in its function. As a result, a particular combination of polygenes with such an allelic polymorphism may thus play a critical role in leading the cascade reaction to develop vasculitis, and also a regular variation of systemic vasculitis. This is designated as the polygene network in systemic vasculitis. (J Jpn Coll Angiol, 2009, 49: 11-16).