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系统性红斑狼疮患者中白细胞介素-23和白细胞介素-12亚基的表达失调。

Dysregulated expression of interleukin-23 and interleukin-12 subunits in systemic lupus erythematosus patients.

作者信息

Huang Xinfang, Hua Jing, Shen Nan, Chen Shunle

机构信息

Joint Molecular Rheumatology Laboratory of Shanghai Ren Ji Hospital and Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences and Shanghai Jiao Tong University, Shanghai, China.

出版信息

Mod Rheumatol. 2007;17(3):220-3. doi: 10.1007/s10165-007-0568-9. Epub 2007 Jun 20.

Abstract

The aim of this study was to investigate the regulation of interleukin (IL)-12 and IL-23 expression in the autoimmune disease, systemic lupus erythematosus (SLE). mRNA from healthy subjects and SLE patients were prepared from peripheral blood mononuclear cells (PBMC) and quantitative real-time polymerase chain reaction was performed to quantify IL-23 specific subunit P19, IL-12 specific subunit P35, and their common subunit P40. IL-12 specific subunit P35 mRNA expression in untreated and treated SLE patients was significantly lower than healthy controls (P = 0.015 and 0.000, respectively). Compared with untreated SLE patients, treatment of SLE patients with corticosteroids or corticosteroids plus another immunosuppressor significantly suppressed P40 and P19 expression (P = 0.002 and 0.015, respectively). The mRNA levels of p19, p40, and p35 in active SLE patients (SLEDAT > 10) were significantly higher compared with those in the inactive SLE patients (SLEDAI <or= 10) (P = 0.000, 0.000, and 0.017, respectively). These results suggest that deficiency of IL-12 and possibly upregulation of IL-23 may contribute to SLE pathogenesis and both cytokines may be therapeutic targets in SLE.

摘要

本研究的目的是调查自身免疫性疾病系统性红斑狼疮(SLE)中白细胞介素(IL)-12和IL-23表达的调控情况。从健康受试者和SLE患者的外周血单个核细胞(PBMC)中提取mRNA,并进行定量实时聚合酶链反应,以量化IL-23特异性亚基P19、IL-12特异性亚基P35及其共同亚基P40。未经治疗和经治疗的SLE患者中IL-12特异性亚基P35 mRNA表达均显著低于健康对照(分别为P = 0.015和0.000)。与未经治疗的SLE患者相比,用皮质类固醇或皮质类固醇加另一种免疫抑制剂治疗SLE患者可显著抑制P40和P19表达(分别为P = 0.002和0.015)。与非活动性SLE患者(SLEDAI≤10)相比,活动性SLE患者(SLEDAT>10)中p19、p40和p35的mRNA水平显著更高(分别为P = 0.000、0.000和0.017)。这些结果表明,IL-12的缺乏以及可能的IL-23上调可能促成SLE的发病机制,且这两种细胞因子可能都是SLE的治疗靶点。

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