Gloudemans Anouk K, Lambrecht Bart N, Smits Hermelijn H
Department of Pulmonology, Erasmus Medical Center, Rotterdam, The Netherlands.
Clin Dev Immunol. 2013;2013:542091. doi: 10.1155/2013/542091. Epub 2013 Apr 11.
Allergic asthma is characterized by bronchial hyperresponsiveness, a defective barrier function, and eosinophilic lower airway inflammation in response to allergens. The inflammation is dominated by Th2 cells and IgE molecules and supplemented with Th17 cells in severe asthma. In contrast, in healthy individuals, allergen-specific IgA and IgG4 molecules are found but no IgE, and their T cells fail to proliferate in response to allergens, probably because of the development of regulatory processes that actively suppress responses to allergens. The presence of allergen-specific secretory IgA has drawn little attention so far, although a few epidemiological studies point at a reverse association between IgA levels and the incidence of allergic airway disease. This review highlights the latest literature on the role of mucosal IgA in protection against allergic airway disease, the mechanisms described to induce secretory IgA, and the role of (mucosal) dendritic cells in this process. Finally, we discuss how this information can be used to translate into the development of new therapies for allergic diseases based on, or supplemented with, IgA boosting strategies.
过敏性哮喘的特征是支气管高反应性、屏障功能缺陷以及对过敏原产生嗜酸性粒细胞性下气道炎症。这种炎症以Th2细胞和IgE分子为主导，在重症哮喘中还伴有Th17细胞。相比之下，在健康个体中，可发现过敏原特异性IgA和IgG4分子，但没有IgE，并且他们的T细胞对过敏原不发生增殖反应，这可能是由于积极抑制对过敏原反应的调节过程的发展。尽管一些流行病学研究指出IgA水平与过敏性气道疾病发病率之间存在负相关，但迄今为止，过敏原特异性分泌型IgA的存在很少受到关注。本综述重点介绍了关于黏膜IgA在预防过敏性气道疾病中的作用、诱导分泌型IgA的机制以及（黏膜）树突状细胞在此过程中的作用的最新文献。最后，我们讨论了如何利用这些信息转化为基于IgA增强策略或辅以IgA增强策略的过敏性疾病新疗法的开发。
