Marques Cintia Rodrigues, Costa Ryan Santos, Costa Gustavo Nunes de Oliveira, da Silva Thiago Magalhães, Teixeira Tatiane Oliveira, de Andrade Emília Maria Medeiros, Galvão Alana A, Carneiro Valdirene Leão, Figueiredo Camila Alexandrina
Instituto de Ciências da Saúde, Universidade Federal da Bahia, Avenida Reitor Miguel Calmon, s/n, Canela, CEP - 40110-100 Salvador, Bahia Brazil.
Instituto de Saúde Coletiva, Universidade Federal da Bahia, Salvador, Brazil.
Asthma Res Pract. 2015 Oct 20;1:10. doi: 10.1186/s40733-015-0012-4. eCollection 2015.
Multiple factors interact to trigger allergic diseases, including individual genetic background and factors related to the environment such as exposure to allergens, air pollution and respiratory infections. The FOXP3 transcription factor is constitutively expressed in CD4CD25FOXP3 regulatory T cells (Tregs) and is critical for the maintenance of immune homeostasis. For example, FOXP3 is responsible for the suppression of the Th2 response following exposure to allergens. Studies have shown that expression of the gene is reduced in patients with asthma and allergies compared to healthy controls. Therefore, the impairment of FOXP3 function caused by genetic polymorphisms and/or epigenetic mechanisms may be involved in the etiology of asthma and other allergic diseases. This review discusses some aspects of the role of FOXP3 in the development of asthma and allergy, with a particular emphasis on genetic and epigenetic factors.
多种因素相互作用引发过敏性疾病，包括个体遗传背景以及与环境相关的因素，如接触过敏原、空气污染和呼吸道感染。FOXP3转录因子在CD4CD25FOXP3调节性T细胞（Tregs）中持续表达，对维持免疫稳态至关重要。例如，FOXP3负责在接触过敏原后抑制Th2反应。研究表明，与健康对照相比，哮喘和过敏患者中该基因的表达降低。因此，由基因多态性和/或表观遗传机制导致的FOXP3功能受损可能参与哮喘和其他过敏性疾病的病因。本综述讨论了FOXP3在哮喘和过敏发生发展中的作用的一些方面，特别强调了遗传和表观遗传因素。
