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首页> 外文期刊>Allergy >T-cell activation genes differentially expressed at birth in CD4 + T-cells from children who develop IgE food allergy
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T-cell activation genes differentially expressed at birth in CD4 + T-cells from children who develop IgE food allergy

机译：T细胞活化基因在出生时在患有IgE食物过敏的儿童的CD4 + T细胞中差异表达

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Background: Presymptomatic immaturity in neonatal T-cell function is a consistent antecedent of allergic disease, including reduced responsiveness to polyclonal activation. Methods: To elucidate the underlying mechanisms, we examined for differences in T-cell gene expression in longitudinal samples collected at birth and at 1 year of age in children with (n = 30) and without IgE-mediated food allergy (n = 30). We employed a low-level soluble anti-CD3 stimulus to activate the T-cell receptor (TCR) and surveyed gene expression by DNA microarray in purified CD4 + T-cells. Allergen-specific responses were assessed in parallel functional studies. Results: At birth, the allergic group showed a reduced number of genes up regulated in response to anti-CD3 treatment on the microarray and a reduced lympho proliferative capacity, suggesting clear differences in T-cell signalling pathways. Polymerase chain reaction (PCR) validation of candidate genes confirmed significantly lower expression of a number of genes in the allergic group including RELB, NFKB2, LIF and FAS. By 12 months of age, there were marked changes in the anti-CD3 response in all infants, culminating in upregulation of cytokine genes (IL-5, IL-13, IL-17 and IL-22). Neonatal differences were no longer apparent. Instead, the allergic group, all symptomatic by this age, showed differential expression of T-cell lineage pathways including GATA-3, MAL and FcER1 in unstimulated T-cells. Allergen stimulation induced significantly higher cytokines production (IL-5, IL-13 and IFNγ) in the allergic group. Conclusion: Although transient, suboptimal neonatal T-cell activation pathways that signal through the NF-κB complex may affect the developmental transition of T-cell phenotypes in the periphery shortly after birth and may increase the risk of food allergy.
机译：背景：新生儿T细胞功能的症状前不成熟是过敏性疾病的一贯先决条件，包括对多克隆激活的反应性降低。方法：为阐明其潜在机制，我们检查了患有（n = 30）和没有IgE介导的食物过敏（n = 30）的儿童在出生时和1岁时收集的纵向样品中T细胞基因表达的差异。 。我们采用了低水平的可溶性抗CD3刺激来激活T细胞受体（TCR），并通过DNA芯片检测了纯化的CD4 + T细胞中的基因表达。在平行功能研究中评估了过敏原特异性反应。结果：出生时，变态反应组的微阵列上抗CD3处理的基因上调的基因数量减少，淋巴细胞的增殖能力降低，表明T细胞信号传导途径存在明显差异。候选基因的聚合酶链反应（PCR）验证证实了过敏组中包括RELB，NFKB2，LIF和FAS在内的许多基因的表达明显降低。到12个月大时，所有婴儿的抗CD3反应都发生了明显变化，最终导致细胞因子基因（IL-5，IL-13，IL-17和IL-22）的上调。新生儿差异不再明显。取而代之的是，这个年龄段的所有变态反应的过敏组在未刺激的T细胞中显示出T细胞谱系通路（包括GATA-3，MAL和FcER1）的差异表达。过敏原刺激在过敏组中诱导明显更高的细胞因子产生（IL-5，IL-13和IFNγ）。结论：尽管通过NF-κB复合物发出短暂，次佳的新生儿T细胞活化途径可能会影响出生后不久外周的T细胞表型的发育转变，并可能增加食物过敏的风险。

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