IL-22促进了原发性干燥综合征唾液腺炎症的发生
发表者：李常虹
日期：2015-03-07
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摘要（意大利）：目的：在慢性炎性疾病中，IL-2即可作为一种保护性细胞因子，也可作为一种促炎性细胞因子发挥作用。在粘膜部位，IL-22主要由CD4+T细胞和表达NKP44受体的自然杀伤细胞(NKp44 + NK )产生。本研究的主要目的是检测原发性干燥综合征（pSS）患者唾液腺中IL-22的表达情况。
方法：对19例pSS患者和16例非特异性慢性唾液腺炎患者进行小唾液腺活检。应用real-time PCR和免疫组化的方法检测实验组与对照组患者唾液腺中IL-17，IL-22，IL-23 以及信号转导和转录激活因子3(STAT3)的基因表达情况。同时在唾液腺浸润的炎性细胞中，采用荧光激活细胞排序分析与免疫组化的方法检测IL-22的细胞来源。
结果：在蛋白质和mRNA水平上，IL-22，IL-23及IL-17 在pSS患者唾液腺中表达均明显升高。STAT3的mRNA及酪氨酸磷酸化蛋白的水平也在pSS患者唾液腺中表达均明显升高。而pSS患者中，Th17细胞和NKp44 + NK 细胞是IL-22的主要细胞来源。
结论：我们的实验结果表明，IL-22联合IL-17、IL-23在pSS的发病机制中起到了一定的促炎作用。
附原文：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 fl uorescence-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-infl ammatory role in the pathogenesis of pSS.
引自：Francesco Ciccia, Giuliana Guggino, Aroldo Rizzo, Angelo Ferrante, Stefania Raimondo, AnnaRita Giardina, Francesco Dieli, Giuseppina Campisi, Riccardo Alessandro, Giovanni Triolo.Potential involvement of IL-22 and IL-22-producing cells in the inflamed salivary glands of patients with Sjögren’s syndrome. Ann Rheum Dis 2012;71:295–301.Doi:10.1136/ard.201 1.154013 （注：干燥综合症病人或亲属可加QQ群交流，群号： 118194945 ，本网站站长私人微信号： ssgzz88 ）
方法：对19例pSS患者和16例非特异性慢性唾液腺炎患者进行小唾液腺活检。应用real-time PCR和免疫组化的方法检测实验组与对照组患者唾液腺中IL-17，IL-22，IL-23 以及信号转导和转录激活因子3(STAT3)的基因表达情况。同时在唾液腺浸润的炎性细胞中，采用荧光激活细胞排序分析与免疫组化的方法检测IL-22的细胞来源。
结果：在蛋白质和mRNA水平上，IL-22，IL-23及IL-17 在pSS患者唾液腺中表达均明显升高。STAT3的mRNA及酪氨酸磷酸化蛋白的水平也在pSS患者唾液腺中表达均明显升高。而pSS患者中，Th17细胞和NKp44 + NK 细胞是IL-22的主要细胞来源。
结论：我们的实验结果表明，IL-22联合IL-17、IL-23在pSS的发病机制中起到了一定的促炎作用。
附原文：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 fl uorescence-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-infl ammatory role in the pathogenesis of pSS.
引自：Francesco Ciccia, Giuliana Guggino, Aroldo Rizzo, Angelo Ferrante, Stefania Raimondo, AnnaRita Giardina, Francesco Dieli, Giuseppina Campisi, Riccardo Alessandro, Giovanni Triolo.Potential involvement of IL-22 and IL-22-producing cells in the inflamed salivary glands of patients with Sjögren’s syndrome. Ann Rheum Dis 2012;71:295–301.Doi:10.1136/ard.201 1.154013 （注：干燥综合症病人或亲属可加QQ群交流，群号： 118194945 ，本网站站长私人微信号： ssgzz88 ）