对特应性皮肤损伤进行的大规模DNA微阵列分析显示，在替代途径中表皮分化基因簇过表达，而在角质包膜中缺乏保护性基因表达。
Large-scale DNA microarray analysis of atopic skin lesions shows overexpression of an epidermal differentiation gene cluster in the alternative pathway and lack of protective gene expression in the cornified envelope.
作者信息
Sugiura H, Ebise H, Tazawa T, Tanaka K, Sugiura Y, Uehara M, Kikuchi K, Kimura T
机构信息
Department of Dermatology, Shiga University of Medical Science, Seta Otsu 520-2192, Japan.
出版信息
Br J Dermatol. 2005 Jan;152(1):146-9. doi: 10.1111/j.1365-2133.2005.06352.x.
BACKGROUND
Atopic dermatitis (AD)-specific genes have not yet been clarified. Objectives To identify gene expression specific to active atopic skin lesions.
METHODS
We analysed 23,000 genes in skin biopsy samples from 17 patients with AD and four normal controls using Affymetrix oligonucleotide arrays.
RESULTS
Four of the 10 genes with the greatest differences in expression between patients and controls, S100A8 and S100A7 (upregulated), and loricrin and filaggrin (downregulated), were epidermal differentiation genes located on 1q21, a locus previously reported to have a genetic linkage with AD.
CONCLUSIONS
Our results, showing downregulation of the cornified envelope genes and upregulation of the alternative keratinization pathway, are the first to suggest abnormal epidermal differentiation and defective defences as key abnormalities in AD.
背景
特异性皮炎（AD）相关基因尚未明确。目的：识别活动性特异性皮肤损伤的基因表达。
方法
我们使用Affymetrix寡核苷酸阵列分析了17例AD患者和4例正常对照者皮肤活检样本中的23000个基因。
结果
患者与对照者之间表达差异最大的10个基因中的4个，即S100A8和S100A7（上调），以及兜甲蛋白和丝聚蛋白（下调），是位于1q21的表皮分化基因，该位点先前报道与AD存在遗传连锁。
结论
我们的结果显示角质包膜基因下调和替代性角质化途径上调，首次表明表皮分化异常和防御缺陷是AD的关键异常。
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