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首页> 外文期刊>Allergy >Quantitative profiling of cytokines and chemokines in DOCK8-deficient and atopic dermatitis patients
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Quantitative profiling of cytokines and chemokines in DOCK8-deficient and atopic dermatitis patients

机译：Dock8缺陷和特应性皮炎患者细胞因子和趋化因子的定量分析

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Background Hyper-IgE syndromes (HIES) are a clinically overlapping, heterogeneous group of inborn errors of immunity characterized by elevated serum IgE level, eosinophilia, atopy, and immune dysregulation. Deficiency of DOCK8 protein is potentially a life-threatening autosomal recessive HIES and only curable with bone marrow transplantation. Hence, the diagnosis of DOCK8 deficiency is critical and should be sought at an early stage to initiate definitive therapy. Methods Serum samples from patients with DOCK8 deficiency and atopic dermatitis were profiled on a cytokine/chemokine panel for potential differential expression. Results CXCL10 and TNF-A were upregulated in DOCK8 patients when compared to AD, possibly contributing toward increased susceptibility to infections and cancer. In contrast, epidermal growth factor (EGF) was significantly downregulated in a subgroup of DOCK8-deficient and AD patients, while IL-31 expression was comparable between both DOCK8-deficient and AD cohorts, possibly contributing toward pruritus seen in both groups. Conclusion This comprehensive cytokine profile in HIES patients reveals distinctive biomarkers that differentiate between the DOCK8-deficient and AD patients. The unique expression profile of various inflammatory cytokines in patients with DOCK8 deficiency vs atopic dermatitis likely reflects disease-specific perturbations in multiple cellular processes and pathways leading to a predisposition to infections and allergies seen in these patients. These data agree with the role for EGF replacement therapy in EGF-deficient individuals with AD as well as DOCK8 deficiency through a potential shared pathway. In addition, these novel biomarkers may be potentially useful in distinguishing DOCK8 deficiency from AD allowing early-targeted treatment options.
机译：背景技术Hyper-IgE综合征（Hies）是一种临床重叠，异质的异构误差，其特征在于血清IgE水平升高，嗜酸性粒细胞，特拉特和免疫诱导。 Dock8蛋白的缺乏可能是危及生命的常染色体隐性物质，并且只能用骨髓移植治愈。因此，Dock8缺乏的诊断至关重要，应在早期阶段寻求启动明确疗法。方法对缺乏患者的血清样本和特应性皮炎的血清样本在细胞因子/趋化因子面板上分析了潜在的差异表达。结果与广告相比，在Dock8患者中，CXCL10和TNF-A的上调，可能导致对感染和癌症的易感性增加。相反，表皮生长因子（EGF）在Dock8缺陷和AD患者的亚组中显着下调，而IL-31表达在Dock8缺陷和AD队列之间具有相当的相当，可能导致两组中所见的瘙痒症。结论HIES患者中的这种综合细胞因子概况揭示了区分Dock8缺陷和AD患者的独特生物标志物。 Dock8缺陷患者的各种炎症细胞因子的独特表达谱与特应性皮炎可能反映了多种细胞过程中的疾病特异性扰动，导致这些患者中观察到的感染和过敏的途径。这些数据同意EGF替代疗法在EGF缺陷疗法中的作用，通过潜在的共用路径以及Dock8缺乏。此外，这些新的生物标志物可能在区分Dock8缺乏从允许早期靶向治疗方案的情况下区分Dock8缺乏。

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