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白细胞介素-17A 和白细胞介素-23 在硬斑病中的作用。

Interleukin-17A and interleukin-23 in morphea.

机构信息

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

出版信息

Arch Med Sci. 2012 Dec 20;8(6):1089-95. doi: 10.5114/aoms.2012.32421. Epub 2012 Dec 19.

DOI:10.5114/aoms.2012.32421
PMID:23319986
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3542501/
Abstract

INTRODUCTION

Morphea is a disease included in the group of scleroderma type autoimmune diseases. Interleukin (IL)-17A may play a role at every stage of its pathogenesis. The study aimed at evaluation of IL-17A and IL-23 (as the main cytokine which is supposed to stimulate and maintain synthesis of IL-17) in pathogenesis of morphea.

MATERIAL AND METHODS

The studies were performed on 41 blood samples from patients with morphea. Skin was sampled from 29 patients. The evaluation included: (1) expression of IL-17A and IL-23 genes in peripheral blood mononuclear cells (PBMC) using real-time polymerase chain reaction (PCR), (2) plasma concentrations of IL-17A and IL-23 using ELISA, (3) expression of IL-17A and IL-23 genes in skin using real-time PCR.

RESULTS

The results of gene expression are expressed as median number of copies per million copies of GAPDH. Higher expression of IL-17A has been demonstrated in PBMC of morphea vs. control group (2630 and 1906 respectively; p = 0.004), accompanied by absence of significant differences in its plasma concentration (10 pg/ml in both groups) and by lowered expression in affected skin (9119 and 19113 respectively; p = 0.036). The results failed to demonstrate elevated IL-23 plasma concentration in morphea vs. control group (5 pg/ml and 6 pg/ml respectively; p = 0.335) or its increased expression in the skin (292 vs. 427; p = 0.383), although we noted its increased expression in PBMC (4419 vs. 808; p < 0.001).

CONCLUSIONS

BASED ON THE OBSERVED CORRELATIONS WE SUGGEST THAT: (1) IL-17A does not represent a factor which promotes tissue injury in morphea, (2) IL-23 may playa role in pathogenesis of morphea.

摘要

简介

硬斑病是硬皮病自身免疫性疾病类型之一。白细胞介素(IL)-17A 可能在其发病机制的各个阶段发挥作用。本研究旨在评估白细胞介素-17A 和白细胞介素-23(作为主要细胞因子,刺激和维持白细胞介素-17 的合成)在硬斑病发病机制中的作用。

材料和方法

对 41 例硬斑病患者的血液样本进行了研究。从 29 例患者中采集皮肤样本。评估包括:(1)使用实时聚合酶链反应(PCR)检测外周血单个核细胞(PBMC)中 IL-17A 和 IL-23 基因的表达;(2)使用 ELISA 检测 IL-17A 和 IL-23 的血浆浓度;(3)使用实时 PCR 检测皮肤中 IL-17A 和 IL-23 基因的表达。

结果

基因表达的结果以每百万拷贝 GAPDH 的拷贝数中位数表示。硬斑病患者 PBMC 中 IL-17A 的表达高于对照组(分别为 2630 和 1906;p=0.004),但其血浆浓度无显著差异(两组均为 10pg/ml),受累皮肤中的表达降低(分别为 9119 和 19113;p=0.036)。结果未能证明硬斑病患者的 IL-23 血浆浓度高于对照组(分别为 5pg/ml 和 6pg/ml;p=0.335)或其在皮肤中的表达增加(分别为 292 和 427;p=0.383),尽管我们观察到其在 PBMC 中的表达增加(分别为 4419 和 808;p<0.001)。

结论

基于观察到的相关性,我们提出以下假设:(1)IL-17A 不是硬斑病组织损伤的促进因素;(2)IL-23 可能在硬斑病发病机制中起作用。

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