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首页> 外文期刊>Cytokine >CD4+ T cells from food allergy model are resistant to TCR-dependent apoptotic induction
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CD4+ T cells from food allergy model are resistant to TCR-dependent apoptotic induction

机译：食物过敏模型中的CD4 + T细胞对TCR依赖性凋亡诱导具有抗性

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Background: CD4+ T cell polarization plays a critical role in the pathogenesis of allergy. How to modulate the skewed CD4+ T cell polarization is less clear. The specific immunotherapy (SIT) is the only specific remedy for the treatment of allergic diseases; the therapeutic effect is to be improved. Objectives: This study aims to investigate the role of interleukin (IL)-18 in enhancing the therapeutic effect of SIT. Methods: A peanut allergy mouse model was developed and treated with SIT or/and IL-18. CD4+ T cell apoptosis was assessed by flow cytometry. The expression of Fas ligand (FasL) was observed by quantitative real time RT-PCR and Western blotting. Interferon-gamma in the culture medium was determined by enzyme-linked immunosorbent assay. The fasL gene promoter methylation in CD4+ T cells was assessed by methylation specific PCR. Results: The results showed that lower levels of IL-18 were detected in allergic mice; administration of IL-18 significantly enhanced the therapeutic effect of SIT on suppressing the allergic inflammation in the mouse intestine. In the cell culture studies, IL-18 increased the TCR-dependent CD4+ T cell apoptosis, the expression of FasL in CD4+ T cells, the production of Interferon-gamma and the demethylation of the FasL promoter in CD4+ T cells. Conclusions: Administration of IL-18 enhances the effect of SIT on suppressing allergic inflammation in the mouse intestine via enhancing the TCR-dependent CD4+ T cell apoptosis.
机译：背景：CD4 + T细胞极化在过敏的发病机理中起着至关重要的作用。如何调制偏斜的CD4 + T细胞极化尚不清楚。特异性免疫疗法（SIT）是治疗过敏性疾病的唯一特异性疗法。治疗效果有待提高。目的：本研究旨在探讨白介素（IL）-18在增强SIT治疗效果中的作用。方法：建立花生过敏小鼠模型并用SIT或/和IL-18治疗。通过流式细胞术评估CD4 + T细胞凋亡。通过定量实时RT-PCR和Western印迹观察Fas配体（FasL）的表达。通过酶联免疫吸附测定法测定培养基中的干扰素-γ。通过甲基化特异性PCR评估CD4 + T细胞中的fasL基因启动子甲基化。结果：结果表明，过敏小鼠中IL-18的水平较低; IL-18的施用显着增强了SIT抑制小鼠肠道变应性炎症的治疗效果。在细胞培养研究中，IL-18增加了TCR依赖性CD4 + T细胞凋亡，CD4 + T细胞中FasL的表达，干扰素-γ的产生以及CD4 + T细胞中FasL启动子的去甲基化。结论：IL-18的给药可通过增强TCR依赖性CD4 + T细胞凋亡来增强SIT抑制小鼠肠道过敏性炎症的作用。

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