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Regulatory T cells and asthma.

机译：调节性T细胞和哮喘。

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Airway inflammation in asthma is characterized by activation of T helper type-2 (Th2) T cells, IgE production and eosinophilia. In many cases, this process is related to an inappropriate T cell response to environmental allergens, and other T cell-dependent pathways may also be involved (such as Th17). Regulatory T cells (Tregs) are T cells that suppress potentially harmful immune responses. Two major subsets of Treg are CD25(hi), Foxp3(+)Tregs and IL-10-producing Tregs. There is evidence that the numbers or function of both subsets may be deficient in patients with atopic allergic disease. Recent work has extended these findings into the airway in asthma where Foxp3 expression was reduced and CD25(hi) Treg-suppressive function was deficient. In animal models of allergic airways disease, Tregs can suppress established airway inflammation and airway hyperresponsiveness, and protocols to enhance the development, recruitment and function of Tregs have been described. Together with studies of patients and in vitro studies of human T cells, these investigations are defining potential interventions to enhance Treg function in the airway in asthma. Existing therapies including corticosteroids and allergen immunotherapy act on Tregs, in part to increase IL-10 production, while vitamin D3 and long-acting beta-agonists enhance IL-10 Treg function. Other possibilities may be enhancement of Treg function via histamine or prostanoid receptors, or by blocking pro-inflammatory pathways that prevent suppression by Tregs (activation of Toll-like receptors, or production of cytokines such as IL-6 and TNF-alpha). As Tregs can also suppress the potentially beneficial immune response important for controlling infections and cancer, a therapeutic intervention should target allergen- or site-specific regulation.
机译：哮喘中的气道炎症的特征在于激活T型辅助2型（Th2）T细胞，IgE产生和嗜酸性粒细胞增多。在许多情况下，该过程与对环境变应原的不适当的T细胞反应有关，并且还可能涉及其他T细胞依赖性途径（例如Th17）。调节性T细胞（Tregs）是抑制潜在有害免疫反应的T细胞。 Treg的两个主要子集是CD25（hi），Foxp3（+）Treg和产生IL-10的Treg。有证据表明，特应性变态反应患者的两个亚群的数量或功能可能不足。最近的工作已将这些发现扩展到哮喘的气道中，其中Foxp3表达降低并且CD25（hi）Treg抑制功能不足。在过敏性气道疾病的动物模型中，Treg可抑制已建立的气道炎症和气道高反应性，并且已描述了增强Treg的发育，募集和功能的方案。连同对患者的研究和人类T细胞的体外研究，这些研究正在确定增强哮喘气道Treg功能的潜在干预措施。现有的疗法，包括皮质类固醇和过敏原免疫疗法，对Treg起作用，部分是增加IL-10的产生，而维生素D3和长效β-激动剂则增强IL-10 Treg的功能。其他可能性可能是通过组胺或类前列腺素受体增强Treg功能，或者是通过阻断阻止Treg抑制的促炎途径（激活Toll样受体或产生IL-6和TNF-α等细胞因子）来增强Treg功能。由于Tregs还可以抑制对控制感染和癌症至关重要的潜在有益的免疫反应，因此治疗干预应针对过敏原或位点特异性调节。

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