外周血白细胞介素-22在支气管哮喘患者中的表达及其临床意义

目的 通过分析白细胞介素(IL)-22在支气管哮喘中的表达,探讨IL-22是否参与支气管哮喘的发病机制及与疾病的关系.方法 采用实时定量聚合酶链式反应(Real-time PCR)和酶联免疫吸附试验(ELISA)分别测定对照组(10例)、哮喘组(17例)和哮喘缓解组(16例)中IL-22 mRNA和蛋白的表达.结果 哮喘组患者中IL-22 mRNA和蛋白表达明显高于哮喘缓解组和对照组.它的表达与哮喘患者第1秒用力呼吸容积占预计值百分比(FEV1％)和第1秒用力呼气容积占肺活量比值(FEV1/FVC％)呈负相关,而与哮喘严重程度评分(ASS)呈正相关.结论 IL-22可能在支气管哮喘的发病机制中起到一定作用,且与支气管哮喘的严重程度有一定关系.  

Th17细胞与肝脏疾病

辅助性T细胞（Th细胞）根据产生细胞因子和生物学功能分为Th1和Th2细胞。最近研究发现了一种与Th1和Th2细胞亚群不同的活化CD4^＋T细胞亚群-Th17细胞。TGF-8与IL-6或IL-21的协同作用，诱导Th17细胞分化。IL-12家族的IL-23在促进IL-17分泌、增强Th17细胞效应功能方面发挥重要作用，而RORγt是其特异性转录因子。分化成熟的Th17细胞可以分泌IL-17A、IL-17F、IL-21、IL-22、IL-6、TNF—α等多种细胞因子，在介导炎性反应（防御病原菌感染）、自身免疫性疾病、肿瘤、移植排斥反应等过程中发挥重要作用。Th17细胞也为研究肝脏疾病的发病机制及防治策略提供了新思路和方向。  

Evaluation of Th17-related cytokines and IFNγ production from blood mononuclear cells of moderate and severe asthmatic children reveals methylprednisolone does not decrease IL-22 levels

Objective: The aim of this study was to correlate IL-6, IL-17A, IFNγ, and IL-22 production with asthma disease severity and to evaluate if methylprednisolone downregulated cytokine production in peripheral blood mononuclear cells (PBMCs). Methods: Forty-two children with chronic persistent asthma and 34 non-asthmatic children were selected. Cytokines were quantified by ELISA from serum or PBMCs supernatants, after the PMA and Ionomycin stimulation, with or without methylprednisolone at 100?µM. Results: Our data showed undetectable levels of serum cytokines in most patients and controls. In the PBMCs, we have observed a higher production of IL-17A than IL-22 among asthmatics and controls, although it is not statistically significant. IL-6, IFNγ, and IL-17A levels were significantly reduced after methylprednisolone treatment (p?=?0.02, 0.03, and 0.03, respectively) in Severe Persistent Asthma (SPA) and in Moderate Persistent Asthma (MPA), (p?=?0.007, 0.01, and 0.007, respectively). However, IL-22 levels were unaffected (SPA, p?=?0.12 and MPA, p?=?0.93). Conclusion: Methylprednisolone downregulated IL-6, IL17A, and IFNγ, but not IL-22, in stimulated PBMCs from asthmatic children indicating that methylprednisolone has no effect on IL-22 production by PBMCs.