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FOXP3转录因子在过敏性哮喘免疫调节中的作用

The role of the FOXP3 transcription factor in the immune regulation of allergic asthma.

作者信息

Schmidt-Weber Carsten B, Blaser Kurt

机构信息

Swiss Institute of Allergy and Asthma Research (SIAF), Obere Str. 22, CH-7270 Davos, Switzerland.

出版信息

Curr Allergy Asthma Rep. 2005 Sep;5(5):356-61. doi: 10.1007/s11882-005-0006-z.

Abstract

Unbalanced immune reactions against allergens are caused by Th2 cells, which are the basis of immunoglobulin E (IgE)-mediated symptoms of allergy and asthma. Although Th2 cells are essential for allergy, they are not sufficient to cause disease, because regulatory T cells (Tregs) control their activity and expansion. Therefore, Tregs are assumed to play an important role not only in the sensitization but also in established allergic disease under therapy. A key factor of Tregs is FOXP3, which, upon expression, is sufficient to induce regulatory T-cell phenotypes. The initiation and suppressive function of FOXP3 and Tregs in the context of allergic asthma are discussed in this review.

摘要

针对过敏原的免疫反应失衡是由辅助性T细胞2(Th2细胞)引起的,Th2细胞是免疫球蛋白E(IgE)介导的过敏和哮喘症状的基础。虽然Th2细胞对于过敏至关重要,但它们并不足以引发疾病,因为调节性T细胞(Tregs)会控制其活性和增殖。因此,Tregs不仅在致敏过程中,而且在治疗中的已确诊过敏性疾病中都被认为起着重要作用。Tregs的一个关键因素是叉头框蛋白P3(FOXP3),其一旦表达,就足以诱导调节性T细胞表型。本文综述讨论了FOXP3和Tregs在过敏性哮喘背景下的起始作用和抑制功能。

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