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特应性皮炎患者表皮屏障的结构与功能——治疗选择。第一部分。

Structure and function of the epidermal barrier in patients with atopic dermatitis - treatment options. Part one.

作者信息

Pelc Jagoda, Czarnecka-Operacz Magdalena, Adamski Zygmunt

机构信息

Department of Dermatology and Venereology, Poznan University of Medical Sciences, Poznan, Poland.

出版信息

Postepy Dermatol Alergol. 2018 Feb;35(1):1-5. doi: 10.5114/ada.2018.73159. Epub 2018 Feb 20.

DOI:10.5114/ada.2018.73159
PMID:29599666
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5872242/
Abstract

Atopic dermatitis is a chronic, recurrent inflammatory skin disease, which is frequently familial. The main cause of the disease seems to be a defect of the epidermal barrier resulting from a genetic predisposition concerning the epidermis, functioning of the immune system as well as environmental factors (which are not related to the immune system). Genes responsible for encoding protein S100, filaggrin, proteases and their inhibitors are the main genes related to the problem of epidermal barrier dysfunction. There is a close connection between structural and immunological processes. Increased expression of cytokine Th2 profile belongs to the latter category. The objective of the present paper is to describe the influence of aforementioned factors on epidermis structure and dysfunction which leads to clinical symptoms of atopic dermatitis.

摘要

特应性皮炎是一种慢性复发性炎症性皮肤病,常具有家族性。该病的主要病因似乎是由与表皮、免疫系统功能以及环境因素(与免疫系统无关)相关的遗传易感性导致的表皮屏障缺陷。负责编码蛋白质S100、丝聚合蛋白、蛋白酶及其抑制剂的基因是与表皮屏障功能障碍问题相关的主要基因。结构和免疫过程之间存在密切联系。细胞因子Th2谱的表达增加属于后者。本文的目的是描述上述因素对表皮结构和功能障碍的影响,而这种功能障碍会导致特应性皮炎的临床症状。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d66/5872242/650c71579096/PDIA-35-31632-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d66/5872242/650c71579096/PDIA-35-31632-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d66/5872242/650c71579096/PDIA-35-31632-g001.jpg

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The prevalence of mutations in the gene encoding filaggrin in the population of Polish patients with atopic dermatitis.波兰特应性皮炎患者群体中编码丝聚合蛋白的基因突变发生率。
Postepy Dermatol Alergol. 2016 Apr;33(2):128-33. doi: 10.5114/ada.2016.59156. Epub 2016 May 16.
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Coexistence of 2282del4 FLG gene mutation and IL-18 -137G/C gene polymorphism enhances the risk of atopic dermatitis.
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