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血清白细胞介素-33 水平在过敏性紫癜患者中的升高。

Elevated serum interleukin-33 levels in patients with Henoch-Schönlein purpura.

机构信息

Department of Dermatovenereology, West China Hospital of Sichuan University, No. 37, Guoxue Alley, Chengdu, Sichuan, China.

出版信息

Arch Dermatol Res. 2013 Mar;305(2):173-7. doi: 10.1007/s00403-012-1268-7. Epub 2012 Jul 27.

DOI:10.1007/s00403-012-1268-7
PMID:22836779
Abstract

Henoch-Schönlein purpura (HSP) is the most common systemic vasculitis and is known as an immunoglobulin (Ig) A related immune complex-mediated disease. However, the molecular mechanisms in the development of HSP are not yet fully understood. Herein, we investigated the serum levels of Interleukin (IL)-33 and soluble ST2 (sST2) in HSP patients and their association with disease severity and IgA autoantibodies production. The serum levels of IL-33 and sST2 were measured by double antibody sandwich enzyme-linked immunosorbent assay (ELISA) in the serum of 33 patients with HSP and 22 controls. Serum levels of IgA anti-endothelial cell antibodies (AECA) and IgA anticardiolipin antibodies (ACA) in HSP patients were detected by double antigen sandwich ELISA. Our results indicated that serum levels of IL-33 but not sST2 were significantly elevated in patients with HSP in acute stage and restored to normal levels in convalescent stage. Moreover, serum IL-33 levels were correlated with the severity of HSP and serum concentrations of AECA-IgA and ACA-IgA. Taken together, we show firstly that serum IL-33 is abnormally elevated in HSP patients. IL-33 might be associated with the IgA autoantibodies production in the pathogenesis of HSP.

摘要

过敏性紫癜(HSP)是最常见的全身性血管炎,被认为是一种免疫球蛋白(Ig)A 相关免疫复合物介导的疾病。然而,HSP 发病机制中的分子机制尚不完全清楚。在此,我们研究了 HSP 患者血清中白细胞介素(IL)-33 和可溶性 ST2(sST2)的水平及其与疾病严重程度和 IgA 自身抗体产生的关系。通过双抗体夹心酶联免疫吸附试验(ELISA)检测 33 例 HSP 患者和 22 例对照者血清中 IL-33 和 sST2 的水平。通过双抗原夹心 ELISA 检测 HSP 患者血清中 IgA 抗内皮细胞抗体(AECA)和 IgA 抗心磷脂抗体(ACA)的水平。结果表明,HSP 患者急性期血清 IL-33 水平显著升高,恢复期恢复正常。此外,血清 IL-33 水平与 HSP 的严重程度以及血清 AECA-IgA 和 ACA-IgA 浓度相关。综上所述,我们首次表明 HSP 患者血清 IL-33 异常升高。IL-33 可能与 HSP 发病机制中的 IgA 自身抗体产生有关。

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