Department of Dermatology, Tokyo Women's Medical University, Tokyo, Japan.
Department of Microbiology and Immunology, Tokyo Women's Medical University, Tokyo, Japan.
Eur J Dermatol. 2017 Jun 1;27(3):247-253. doi: 10.1684/ejd.2017.2985.
In the pathogenesis of atopic dermatitis (AD), skin barrier dysfunction and T-helper (Th) type 2 immune reactions play important roles. Alterations in the stratum spinosum of AD have not been studied in much detail. In this study, we investigated the changes of structural proteins and adhesion molecules residing in the stratum spinosum of AD lesional skin, and whether Th2 cytokines including interleukin (IL)-4 and IL-13 alter the expression of these proteins. Skin samples were collected from patients with AD and from healthy controls. Normal human epidermal keratinocytes were cultured and differentiated in the presence or absence of either IL-4 or IL-13 in vitro. The expression of keratin 1, keratin 10, desmoglein 1 and desmocollin 1 was examined by immunofluorescence and western blotting. The expression of these proteins was downregulated in AD lesional skin, and IL-4 and IL-13 were shown to suppress their expression. These results suggest that the stratum spinosum is impaired in AD lesional skin, possibly by Th2 cytokines, which may be involved in the pathogenesis of AD.
在特应性皮炎(AD)的发病机制中,皮肤屏障功能障碍和辅助性 T 细胞(Th)2 型免疫反应起着重要作用。AD 棘层的改变尚未得到详细研究。在这项研究中,我们研究了 AD 病变皮肤棘层中结构蛋白和黏附分子的变化,以及包括白细胞介素(IL)-4 和 IL-13 在内的 Th2 细胞因子是否改变这些蛋白的表达。从 AD 患者和健康对照者中采集皮肤样本。体外培养正常的人表皮角质形成细胞,并在存在或不存在 IL-4 或 IL-13 的情况下进行分化。通过免疫荧光和 Western blot 检测角蛋白 1、角蛋白 10、桥粒芯糖蛋白 1 和桥粒芯胶蛋白 1 的表达。这些蛋白在 AD 病变皮肤中的表达下调,并且 IL-4 和 IL-13 被证明可以抑制其表达。这些结果表明 AD 病变皮肤的棘层受损,可能是由 Th2 细胞因子引起的,这些细胞因子可能参与 AD 的发病机制。