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在化脓性汗腺炎病变中白细胞介素-36 细胞因子表达增加。

Increased expression of the interleukin-36 cytokines in lesions of hidradenitis suppurativa.

机构信息

Department of Dermatology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.

Department of Dermatology, Mie University Graduate School of Medicine, Tsu, Japan.

出版信息

J Eur Acad Dermatol Venereol. 2017 Dec;31(12):2091-2096. doi: 10.1111/jdv.14389. Epub 2017 Aug 29.

Abstract

BACKGROUND

Hidradenitis suppurativa (HS) is a recalcitrant chronic skin disease with poorly understood immunopathogenic mechanisms. Previous studies reported that the interleukin-36 (IL-36) cytokines [IL-36α, IL-36β, IL-36γ and IL-36 receptor antagonists (IL-36RA)] are important players in the pathogenesis of psoriasis (PS).

OBJECTIVE

We aim to determine whether the IL-36 cytokines are upregulated in patients with HS. For this purpose, we analysed local expression and systemic levels of the IL-36 cytokines in patients with HS and compared the results to healthy donors and patients with PS.

METHODS

Skin biopsies from healthy donors and HS and PS patients were analysed for expression of the IL-36 cytokines by immunohistochemistry and semiquantitative real-time PCR. The enzyme-linked immunosorbent assay (ELISA) was used to measure systemic levels of the IL-36 cytokines in the serum of the three donor groups.

RESULTS

The agonists IL-36α, IL-36β and IL-36γ were found to be upregulated in HS both systemically and lesionally, while the IL-36RA was not differently regulated in comparison to healthy donors.

CONCLUSION

Our findings suggest that the agonistic IL-36 isoforms are upregulated in HS. The relevance of the enhanced production of IL-36 cytokines in HS pathogenesis remains to be determined.

摘要

背景

化脓性汗腺炎(HS)是一种难治性慢性皮肤病,其免疫发病机制尚未完全阐明。先前的研究报告称,白细胞介素-36(IL-36)细胞因子[IL-36α、IL-36β、IL-36γ 和 IL-36 受体拮抗剂(IL-36RA)]是银屑病(PS)发病机制中的重要参与者。

目的

我们旨在确定 HS 患者的 IL-36 细胞因子是否上调。为此,我们通过免疫组织化学和半定量实时 PCR 分析了 HS 患者、健康供体和 PS 患者的局部表达和系统水平的 IL-36 细胞因子,并将结果与健康供体和 PS 患者进行了比较。

方法

通过免疫组织化学和半定量实时 PCR 分析健康供体和 HS 和 PS 患者的皮肤活检组织中 IL-36 细胞因子的表达。酶联免疫吸附试验(ELISA)用于测量三组供体血清中 IL-36 细胞因子的系统水平。

结果

发现 HS 患者的激动剂 IL-36α、IL-36β 和 IL-36γ 在全身和病变部位均上调,而与健康供体相比,IL-36RA 的调节没有差异。

结论

我们的发现表明,HS 中激动性 IL-36 同工型上调。IL-36 细胞因子在 HS 发病机制中的增强产生的相关性仍有待确定。

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