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潜在的 IL-22 和产生 IL-22 的细胞参与干燥综合征患者的炎症唾液腺。

Potential involvement of IL-22 and IL-22-producing cells in the inflamed salivary glands of patients with Sjogren's syndrome.

机构信息

Dipartimento Biomedico di Medicina Interna e Specialistiche, Sezione di Reumatologia, Università di Palermo, Italy.

出版信息

Ann Rheum Dis. 2012 Feb;71(2):295-301. doi: 10.1136/ard.2011.154013. Epub 2011 Oct 6.

DOI:10.1136/ard.2011.154013
PMID:21979002
Abstract

OBJECTIVES

In chronic inflammatory disorders, interleukin (IL)-22 may act either as a protective or as a pro-inflammatory cytokine. At mucosal sites, IL-22 is mainly produced by CD4(+) T cells and by a subset of mucosal natural killer (NK) cells expressing the receptor NKp44 (NKp44(+) NK cells). The aim of this study was to investigate the IL-22 expression in the salivary glands of patients with primary Sjögren's syndrome (pSS).

METHODS

Minor salivary gland biopsies were obtained from 19 patients with pSS and 16 with non-specific chronic sialoadenitis. Quantitative gene expression analysis by TaqMan real-time PCR and immunohistochemistry for IL-17, IL-22, IL-23 and STAT3 (signal transducer and activator of transcription) was performed on salivary glands from patients and controls. The cellular sources of IL-22 among infiltrating inflammatory cells were also determined by fluorescence-activated cell sorting analysis and immunohistochemistry.

RESULTS

IL-22, IL-23 and IL-17 were significantly increased at both protein and mRNA levels in the inflamed salivary glands of patients with pSS. STAT3 mRNA and the tyrosine phosphorylated corresponding protein were also significantly increased in pSS. Th17 and NKp44(+) NK cells were the major cellular sources of IL-22 in patients with pSS.

CONCLUSIONS

Our results suggest that, together with IL-17 and IL-23, IL-22 may play a pro-inflammatory role in the pathogenesis of pSS.

摘要

目的

在慢性炎症性疾病中,白细胞介素(IL)-22 可能作为保护性或促炎细胞因子发挥作用。在黏膜部位,IL-22 主要由 CD4+T 细胞和表达受体 NKp44(NKp44+NK 细胞)的黏膜自然杀伤(NK)细胞亚群产生。本研究旨在探讨原发性干燥综合征(pSS)患者唾液腺中 IL-22 的表达情况。

方法

从 19 例 pSS 患者和 16 例非特异性慢性涎腺炎患者中获取小唾液腺活检组织。采用 TaqMan 实时 PCR 和免疫组织化学法检测患者和对照者唾液腺中 IL-17、IL-22、IL-23 和信号转导和转录激活因子 3(STAT3)的基因表达。通过荧光激活细胞分选分析和免疫组织化学法确定浸润性炎症细胞中 IL-22 的细胞来源。

结果

pSS 患者炎症唾液腺中 IL-22、IL-23 和 IL-17 的蛋白和 mRNA 水平均显著升高。pSS 患者 STAT3 mRNA 和相应的酪氨酸磷酸化蛋白也显著增加。Th17 和 NKp44+NK 细胞是 pSS 患者 IL-22 的主要细胞来源。

结论

我们的研究结果表明,IL-22 可能与 IL-17 和 IL-23 一起在 pSS 的发病机制中发挥促炎作用。

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