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首页> 外文期刊>Allergy >The functional insufficiency of human CD4+CD25 high T-regulatory cells in allergic asthma is subjected to TNF-alpha modulation.
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The functional insufficiency of human CD4+CD25 high T-regulatory cells in allergic asthma is subjected to TNF-alpha modulation.

机译：人CD4 + CD25高T调节细胞在过敏性哮喘中的功能不足受到TNF-α调节。

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BACKGROUND: Natural CD4(+)CD25(high)Foxp3(+) regulatory T (nTreg) cells are important in maintaining immunologic tolerance, but their role in the pathogenesis of allergic asthma is unclear. We studied the function of nTreg cells in allergic asthmatic children and assessed the factors which may relate to the functional insufficiency of nTreg cells. METHODS: The percentage of CD4(+)CD25(high) Treg cells, the expression of Foxp3, and the cell-induced suppressive activity of nTreg cells isolated from nonatopic controls, allergic asthmatics, and allergen-specific immunotherapy (AIT)-treated asthmatic patients were studied. RESULTS: Although the percentage of nTreg in peripheral blood mononuclear cells was increased, the expression of Foxp3 and its cell-induced suppressive activity were significantly lower in Dermatophagoides pteronyssinus (Der p)-sensitive asthmatic children when compared to nonatopic controls. In contrast, the expression of Foxp3 and the functional activity of nTreg cells were reversed in allergic asthmatics who received AIT. The addition of recombinant tumor necrosis factor (TNF)-alpha directly downregulated Foxp3 expression and abrogated the cell-induced suppressive function of Treg cells. The anti-TNF-alpha reagent, etanercept, restored the functional activity and Foxp3 expression of CD4(+)CD25(high) Treg derived from allergic asthmatics. CONCLUSIONS: The functional insufficiency of nTreg cells in patients with allergic asthma may be related to the enhanced production of TNF-alpha and its effect on the Foxp3 expression. These results may explain, in part, the effectiveness of anti-TNF-alpha therapy in the treatment of allergic asthma.
机译：背景：天然CD4（+）CD25（高）Foxp3（+）调节性T（nTreg）细胞在维持免疫耐受方面很重要，但它们在过敏性哮喘发病机理中的作用尚不清楚。我们研究了过敏性哮喘儿童中nTreg细胞的功能，并评估了可能与nTreg细胞功能不足有关的因素。方法：从非特应性对照，过敏性哮喘和过敏原特异性免疫疗法（AIT）治疗的哮喘患者中分离出CD4（+）CD25（高）Treg细胞百分比，Foxp3的表达以及对nTreg细胞的细胞诱导抑制活性。研究了患者。结果：与非特应性对照组相比，对敏感性皮炎性皮炎（Der pophonyides pteronyssinus（Der p））的儿童，外周血单个核细胞中nTreg的百分比增加，但Foxp3的表达及其细胞抑制活性明显降低。相反，在接受AIT的过敏性哮喘患者中，Foxp3的表达和nTreg细胞的功能活性相反。重组肿瘤坏死因子（TNF）-α的添加直接下调Foxp3表达，并废除了细胞诱导的Treg细胞抑制功能。抗TNF-α试剂etanercept恢复了源自过敏性哮喘的CD4（+）CD25（high）Treg的功能活性和Foxp3表达。结论：过敏性哮喘患者nTreg细胞功能不足可能与TNF-α产生增加及其对Foxp3表达的影响有关。这些结果可以部分解释抗TNF-α疗法在过敏性哮喘治疗中的有效性。

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