claudin-1在银屑病中的表达缺失与角质形成细胞的增殖状态有关

M. Madakshira, B. Radotra, U. Saikia
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引用次数: 0

摘要

背景:银屑病是一种慢性缓解性和复发性炎症性疾病,患病率为0.44%-2.5%,以t细胞介导的上皮细胞快速更新为特征。Claudin-1蛋白是角质形成细胞紧密连接的一个组成部分,在增殖、分化和细胞粘附中起作用。目的:探讨claudin-1表达在银屑病中与角质细胞增殖的关系。材料与方法:选取50例银屑病患者作为研究对象。皮肤活检进行claudin-1和Ki67免疫组化。测定细胞基底层和棘层中Claudin-1的表达。测定Ki67增殖指数。7例正常皮肤活检作为对照。采用费雪精确检验进行统计分析。结果:本组病例年龄广泛(14 ~ 78岁),平均46岁,以男性为主(4:1)。82%的基底细胞层完全丧失claudin-1的表达(n = 42)。棘层显示96%的claudin-1表达减少(n = 48)。claudin-1表达缺失在基底层和棘层之间的相关性有统计学意义(P = 0.0229)。claudin-1表达缺失与Ki67高增殖指数的相关性也有统计学意义(P < 0.00001)。结论:我们的研究表明,在银屑病中,claudin-1在表皮下层的表达持续缺失,而这也是银屑病增殖活性强烈的部位。t细胞释放的细胞因子汤可能导致claudin-1的下调,claudin-1是细胞增殖的触发因素之一。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Loss of expression of claudin-1 in psoriasis is associated with proliferative state of keratinocytes
Background: Psoriasis is a chronic remitting and relapsing inflammatory disease, with a prevalence of 0.44%–2.5% and is characterized by T-cell-mediated rapid turnover of epithelial cells. Claudin-1 protein is an integral part of the keratinocyte tight junction and has a role in proliferation, differentiation, and cell adhesion. Aim: The aim of the study was to investigate the role of claudin-1 expression in relation to keratinocyte proliferation in psoriasis. Materials and Methods: Fifty cases of psoriasis were included in the study. Skin biopsies were subjected to claudin-1 and Ki67 immunohistochemistry. Claudin-1 expression in the basal and spinous layers was scored. Ki67 proliferation index was assessed. Seven cases of normal skin biopsies were also included as controls. Fisher's exact test was applied for statistical analysis. Results: The cases had a wide age range (14–78 years), with a mean of 46 years with a male preponderance (4:1). The basal cell layer showed a complete loss of expression for claudin-1 in 82% (n = 42). The spinous layer showed a decrescendo pattern of loss of claudin-1 expression in 96% (n = 48). The association of loss of expression of claudin-1 between the basal layer and spinous layer was statistically significant (P = 0.0229). The association of loss of expression of claudin-1 and high Ki67 proliferative index was also statistically significant (P < 0.00001). Conclusion: Our study showed consistent loss of expression of claudin-1 in the lower layers of the epidermis in psoriasis, which is also the site of intense proliferative activity. The cytokine soup released by the T-cells may be responsible for downregulation of claudin-1, which is one of the triggers for proliferation.
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