白细胞介素-25对葡萄膜炎-青光眼-交感性眼炎综合征中促炎细胞因子的抑制作用。
Inhibition of proinflammatory cytokine by IL-25 in Vogt-Koyanagi-Harada syndrome.
作者信息
Xu Mei, Wang Chaokui, Tian Yuan, Kijlstra Aize, Yang Peizeng
机构信息
Department of Opthalmology, The First Affiliated Hospital of Chongqing Medical University, Chongqing Key Lab of Ophthalmology, Chongqing Eye Institute , Chongqing , P. R. China .
出版信息
Ocul Immunol Inflamm. 2014 Aug;22(4):294-9. doi: 10.3109/09273948.2013.854391. Epub 2013 Dec 11.
PURPOSE
Vogt-Koyanagi-Harada (VKH) syndrome is a multisystem disorder presumed to be mediated by an autoimmune response. Recent studies have shown that interleukin (IL) 25 was involved in the T-cell immune response. This study analyzed the expression and potential role of IL-25 in the pathogenesis of VKH syndrome.
METHODS
The IL-25 serum levels were determined by enzyme-linked immunosorbent assay (ELISA). The IL-1β, IL-6, and TNF-α level in supernatants of PBMCs cultured with LPS in the absence or presence of recombinant(r) IL-25 was detected by ELISA.
RESULTS
A significantly decreased serum IL-25 level was found in VKH patients. In vitro experiments showed that rIL-25 was able to significantly inhibit the production of IL-1β, IL-6, and TNF-α by PBMCs from active VKH patients.
CONCLUSIONS
IL-25 may be involved in the development of VKH syndrome, possibly by inhibiting the expression of proinflammatory cytokines.
目的
Vogt-小柳-原田（VKH）综合征是一种多系统疾病，推测由自身免疫反应介导。最近的研究表明，白细胞介素（IL）-25参与了T细胞免疫反应。本研究分析了IL-25在VKH综合征发病机制中的表达及潜在作用。
方法
采用酶联免疫吸附测定（ELISA）法测定血清IL-25水平。用ELISA法检测在有无重组（r）IL-25情况下，脂多糖（LPS）刺激外周血单个核细胞（PBMCs）培养上清液中IL-1β、IL-6和肿瘤坏死因子-α（TNF-α）的水平。
结果
VKH患者血清IL-25水平显著降低。体外实验表明，rIL-25能够显著抑制活动期VKH患者PBMCs产生IL-1β、IL-6和TNF-α。
结论
IL-25可能参与VKH综合征的发病过程，可能是通过抑制促炎细胞因子的表达来实现的。
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