IL-33-ST2轴参与了原发性干燥综合征的发病
发表者：北京市海淀医院 费雅楠
日期：2015-02-27
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摘要: 目的 为了研究白介素（IL）-33-ST2轴在原发性干燥综合征（pSS）病理生理中的作用。
方法: 用ELISA的方法测定血清中IL-33和sST2的水平。用免疫组化的方法测定唾液腺（SG）IL-33和ST2的表达。PBMC被分离和刺激成IL-33、IL-12和IL23，用流式细胞仪对细胞因子谱反应进行检测。用流式细胞仪检测细胞内细胞因子INFγ和IL-17。
结果:原发性干燥综合征患者和对照组及系统性红斑狼疮患者相比血清IL-33和sST2的水平增加。唾液腺Chisholm评分2-3分的原发性干燥综合征患者与对照组唾液腺Chisholm评分4分的相比IL-33的表达上调。原发性干燥综合征患者唾液腺ST2的表达下调。IL-33在不同浓度并没有增加促炎细胞因子的分泌，而是协同作用IL-12和IL-23以促进IFNγ的产生。NK和NKT细胞被确定为体外IFNγ的主要生产者，并且在原发性干燥综合征患者的唾液腺中可以发现。
结论:在原发性干燥综合征通过NK和NKT细胞IL-33释放和作用于IL-12和IL-23以有利于IFNγ的分泌。
附原文:ABSTRACT Objectives To investigate the role of the interleukin (IL)-33–ST2 axis in the pathophysiology of primary Sjögren’s syndrome ( pSS). Methods Serum levels of IL-33 and sST2 were determined by ELISA. The expression of IL-33 and ST2 was investigated in salivary glands (SG) by immunohistochemistry. PBMC were isolated and stimulated with IL-33, IL-12 and IL-23 and the cytokine profile response was examined by flow cytometry.Intracellular cytokine detection of IFNγ and IL-17 was performed by flow cytometry.Results Serum IL-33 and sST2 levels were increased in pSS patients compared with controls and patients with systemic lupus erythematosus. Expression of IL-33 was upregulated in SG with Chisholm scores of 2 and 3 of pSS patients but comparable with controls for SG with Chisholm score of 4. ST2 expression in SG was downregulated in pSS patients. IL-33 at different concentrations did not increase the secretion of proinflammatory cytokines but acted synergistically with IL-12 and IL-23 to promote IFNγ production. NK and NKT cells were identified as main producers of IFNγ in vitro and were found in SG of pSS patients.Conclusions IL-33 is released in pSS, and acts with IL-12 and IL-23 to favour the secretion of IFNγ by NK and NKT cells.
引自：Ahmad A,et al. Potential involvement of the IL-33–ST2 axis in the pathogenesis of primary Sjögren’s syndrome. Ann Rheum Dis 2014;73:1259–1263. doi:10.1136/annrheumdis-2012-203187. （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: 用ELISA的方法测定血清中IL-33和sST2的水平。用免疫组化的方法测定唾液腺（SG）IL-33和ST2的表达。PBMC被分离和刺激成IL-33、IL-12和IL23，用流式细胞仪对细胞因子谱反应进行检测。用流式细胞仪检测细胞内细胞因子INFγ和IL-17。
结果:原发性干燥综合征患者和对照组及系统性红斑狼疮患者相比血清IL-33和sST2的水平增加。唾液腺Chisholm评分2-3分的原发性干燥综合征患者与对照组唾液腺Chisholm评分4分的相比IL-33的表达上调。原发性干燥综合征患者唾液腺ST2的表达下调。IL-33在不同浓度并没有增加促炎细胞因子的分泌，而是协同作用IL-12和IL-23以促进IFNγ的产生。NK和NKT细胞被确定为体外IFNγ的主要生产者，并且在原发性干燥综合征患者的唾液腺中可以发现。
结论:在原发性干燥综合征通过NK和NKT细胞IL-33释放和作用于IL-12和IL-23以有利于IFNγ的分泌。
附原文:ABSTRACT Objectives To investigate the role of the interleukin (IL)-33–ST2 axis in the pathophysiology of primary Sjögren’s syndrome ( pSS). Methods Serum levels of IL-33 and sST2 were determined by ELISA. The expression of IL-33 and ST2 was investigated in salivary glands (SG) by immunohistochemistry. PBMC were isolated and stimulated with IL-33, IL-12 and IL-23 and the cytokine profile response was examined by flow cytometry.Intracellular cytokine detection of IFNγ and IL-17 was performed by flow cytometry.Results Serum IL-33 and sST2 levels were increased in pSS patients compared with controls and patients with systemic lupus erythematosus. Expression of IL-33 was upregulated in SG with Chisholm scores of 2 and 3 of pSS patients but comparable with controls for SG with Chisholm score of 4. ST2 expression in SG was downregulated in pSS patients. IL-33 at different concentrations did not increase the secretion of proinflammatory cytokines but acted synergistically with IL-12 and IL-23 to promote IFNγ production. NK and NKT cells were identified as main producers of IFNγ in vitro and were found in SG of pSS patients.Conclusions IL-33 is released in pSS, and acts with IL-12 and IL-23 to favour the secretion of IFNγ by NK and NKT cells.
引自：Ahmad A,et al. Potential involvement of the IL-33–ST2 axis in the pathogenesis of primary Sjögren’s syndrome. Ann Rheum Dis 2014;73:1259–1263. doi:10.1136/annrheumdis-2012-203187. （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 ）