Chang Jen-Chieh, Wang Lin, Chen Rong-Fu, Liu Chieh-An
Institute of Biomedical Sciences, National Sun Yat-Sen University, Kaohsiung 804, Taiwan.
Clin Dev Immunol. 2012;2012:270869. doi: 10.1155/2012/270869. Epub 2012 Feb 28.
Atopic asthma is a complex disease associated with IgE-mediated immune reactions. Numerous genome-wide studies identified more than 100 genes in 22 chromosomes associated with atopic asthma, and different genetic backgrounds in different environments could modulate susceptibility to atopic asthma. Current knowledge emphasizes the effect of tobacco smoke on the development of childhood asthma. This suggests that asthma, although heritable, is significantly affected by gene-gene and gene-environment interactions. Evidence has recently shown that molecular mechanism of a complex disease may be limited to not only DNA sequence differences, but also gene-environmental interactions for epigenetic difference. This paper reviews and summarizes how gene-gene and gene-environment interactions affect IgE production and the development of atopic asthma in prenatal and childhood stages. Based on the mechanisms responsible for perinatal gene-environment interactions on IgE production and development of asthma, we formulate several potential strategies to prevent the development of asthma in the perinatal stage.
特应性哮喘是一种与IgE介导的免疫反应相关的复杂疾病。众多全基因组研究在22条染色体上鉴定出100多个与特应性哮喘相关的基因，不同环境中的不同遗传背景可调节对特应性哮喘的易感性。目前的知识强调烟草烟雾对儿童哮喘发展的影响。这表明哮喘虽然具有遗传性，但受基因-基因和基因-环境相互作用的显著影响。最近有证据表明，复杂疾病的分子机制可能不仅限于DNA序列差异，还包括基因-环境相互作用导致的表观遗传差异。本文综述并总结了基因-基因和基因-环境相互作用如何影响产前和儿童期IgE产生以及特应性哮喘的发展。基于围产期基因-环境相互作用对IgE产生和哮喘发展的作用机制，我们制定了几种预防围产期哮喘发展的潜在策略。
