过敏刺激和糖皮质激素对CD4+T细胞中miR-155的影响。

IF 1.4 Q4 IMMUNOLOGY American journal of clinical and experimental immunology Pub Date : 2018-08-20 eCollection Date: 2018-01-01
Elizabeth Daniel, Alanna Roff, Man-Hsun Hsu, Ronaldo Panganiban, Kristin Lambert, Faoud Ishmael
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摘要

理由:微小RNA(miRNA)正在成为过敏性炎症的重要调节因子和潜在的治疗靶点。我们试图确定哪些miRNA在CD4+T细胞中表达,并确定过敏刺激或糖皮质激素是否改变了它们的表达。方法:在IRB批准后,从尘螨(DM)过敏性鼻炎受试者(n=20)、非过敏性对照者(n=8)和哮喘患者(n=16)中采集血液。外周血单核细胞与尘螨提取物(DME)、稀释剂对照或DME+地塞米松(0.1µM)一起孵育。通过磁珠柱收集CD4+T细胞,并通过胍/苯酚-氯仿提取分离RNA。结果:我们鉴定出196个miRNA在循环CD4+T细胞中稳定表达。与非过敏性受试者相比,用DME刺激CD4+T细胞的过敏原在DM过敏受试者的细胞中差异诱导miR-155表达。用抗CD3/抗CD28模拟和佛波醇-12-嘧啶酸盐13-乙酸酯(PMA)处理也观察到miR-155表达的诱导,并在后一种处理中通过无孔钙和溴环AMP进一步增强。miR-155的表达水平与TH2细胞因子IL-5和IL-13的表达呈正相关。Jurkat T细胞中miR-155的抑制抑制了这些细胞因子的产生。糖皮质激素减弱了尘螨过敏原的作用,增加了抑制这种miRNA可能是糖皮质激素发挥抗炎作用的机制的可能性。CD4+T细胞在哮喘中的miR-155表达水平高于过敏性鼻炎和非哮喘患者。糖皮质激素对CD4+T细胞miR-155表达的抑制作用在严重哮喘患者中消失。结论:Mir-155在暴露于DM提取物的过敏性T细胞中与非过敏性细胞相比有差异表达,并且受到糖皮质激素的抑制。MiR-155可能在介导T细胞的过敏性炎症中发挥作用,并且可能是类固醇的抗炎靶点。这种途径可能在严重哮喘中被解除调节。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Effects of allergic stimulation and glucocorticoids on miR-155 in CD4+ T-cells.

Rationale: MicroRNAs (miRNAs) are emerging as important regulators of allergic inflammation and potential therapeutic targets. We sought to identify which miRNAs are expressed in CD4+ T-cells and determine whether allergic stimuli or glucocorticoids alter their expression.

Methods: After IRB approval, blood was collected from dust mite (DM) allergic rhinitis subjects (n=20), non-allergic controls (n=8), and asthmatics (n=16). Peripheral blood mononuclear cells were incubated with dust mite extract (DME), diluent control, or DME + dexamethasone (0.1 µM). CD4+ T-cells were collected by magnetic bead column, and RNA was isolated by guanidinium/phenol-chloroform extraction. MicroRNA expression was measured using Nanostring microarray and quantitative real time PCR (qPCR).

Results: We identified 196 miRNAs that were stably expressed in circulating CD4+ T-cells. Allergen stimulation of CD4+ T-cells with DME differentially induced miR-155 expression in cells of DM-allergic subjects as compared to non-allergic subjects. Induction of miR-155 expression was also observed with anti-CD3/anti-CD28 simulation and phorbol-12-Myristate-13-Acetate (PMA) treatment, and further augmented by calcium inophore and bromocyclic AMP in the latter treatment. The level of miR-155 expression was positively associated with expression of the TH2 cytokines IL-5 and IL-13. Inhibition of miR-155 in Jurkat T-cells inhibited the production of these cytokines. Glucocorticoids attenuated the effects of dust mite allergen, raising the possibility that inhibition of this miRNA could be a mechanism through which glucocorticoids exhibit their anti-inflammatory effects. The CD4+ T-cells had a higher level of miR-155 expression in asthma compared to in allergic rhinitis and non-asthmatics. The inhibitory effects of glucocorticoids on CD4+ T-cell miR-155 expression were lost in severe asthmatics.

Conclusion: Mir-155 is differentially expressed in allergic T-cells exposed to DM extract compared to in non-allergic cells and it is inhibited by glucocorticoids. MiR-155 may play a role in mediating allergic inflammation in T-cells and could be an anti-inflammatory target of steroids. This pathway may be de-regulated in severe asthma.

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