Department of Allergy and Clinical Immunology, National Heart and Lung Institute at Imperial College London, Exhibition Road, London SW7 2AZ, England, UK.
Adv Exp Med Biol. 2009;665:180-94. doi: 10.1007/978-1-4419-1599-3_14.
Allergic diseases such as asthma, rhinitis and eczema are increasing in prevalence worldwide, in particular in industrialised countries affecting up to 20% of the population. Regulatory T-cells (Tregs) have been shown to be critical in T-cell homeostasis and in the maintenance of immune responses, such as prevention of autoimmunity and hampering allergic diseases. The so-called 'natural' CD4+CD25+ Tregs and/or IL-10-producing Tr1 cells have been shown to be responsible for the protection of immune tolerance and intact immune reactions following exposure to allergens such as aeroallergens or food allergens. In this regard, both cell-cell contact (through membrane bound TGF-beta or via suppressive molecules such as CLTA-4) and soluble cytokine-(TGF-beta and IL-10) dependent mechanisms have been shown to contribute to the ability of Tregs to operate effectively. The transcription factor Foxp3, a member of the forkhead-winged helix family, appears to be critical in the suppressive abilities of regulatory T-cells. Adoptive transfer of CD4+CD25+ Tregs from healthy to diseased animals corroborated and provided further evidence of the vital role of these populations in the prevention or cure of certain autoimmune conditions. Clinical improvement seen after allergen immunotherapy for allergic diseases such as rhinitis and asthma has also been associated with the induction of IL-10 and TGF-beta producing Trl cells as well as Foxp3 expressing CD4+CD25+ T-cells, resulting in the suppression ofTh2 cytokine milieu. Activation and expansion ofantigen-specific CD4+CD25+ Tregs in vivo using adjuvants such as IL-10 or pharmacological agents such as low dose steroids or vitamin D3 could represent novel approaches to induce antigen-specific tolerance in immune-mediated conditions such as allergic asthma, autoimmune disease and the rejection of transplanted organs in man.
过敏疾病（如哮喘、鼻炎和湿疹）在全球范围内的发病率不断上升，尤其是在工业化国家，发病率高达 20%。调节性 T 细胞（Tregs）已被证明在 T 细胞稳态和维持免疫反应（如预防自身免疫和阻碍过敏疾病）中至关重要。所谓的“天然”CD4+CD25+Tregs 和/或产生 IL-10 的 Tr1 细胞已被证明负责保护免疫耐受和完整的免疫反应，如暴露于过敏原（如空气过敏原或食物过敏原）后。在这方面，细胞间接触（通过膜结合的 TGF-β或通过抑制分子如 CLTA-4）和可溶性细胞因子（TGF-β和 IL-10）依赖性机制都被证明有助于 Tregs 有效地发挥作用。转录因子 Foxp3 是叉头翼螺旋家族的一员，似乎对调节性 T 细胞的抑制能力至关重要。从健康动物向患病动物过继转移 CD4+CD25+Tregs 证实并进一步证明了这些群体在预防或治疗某些自身免疫疾病中的重要作用。过敏性疾病（如鼻炎和哮喘）的过敏原免疫治疗后观察到的临床改善也与诱导产生 IL-10 和 TGF-β的 Trl 细胞以及表达 Foxp3 的 CD4+CD25+T 细胞有关，导致 Th2 细胞因子环境的抑制。使用佐剂（如 IL-10）或药理学药物（如低剂量类固醇或维生素 D3）在体内激活和扩增抗原特异性 CD4+CD25+Tregs 可能代表在免疫介导的疾病（如过敏性哮喘、自身免疫性疾病和移植器官排斥）中诱导抗原特异性耐受的新方法。
