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Clinical and Developmental Immunology
Volume 2013, Article ID 542091, 12 pages
Review Article

Potential of Immunoglobulin A to Prevent Allergic Asthma

1Department of Pulmonology, Erasmus Medical Center, Rotterdam, The Netherlands
2Leiden Immunoparasitology Group, Department of Parasitology, Leiden University Medical Center, Albinusdreef 2, P4-37A, 2333 ZA Leiden, The Netherlands
3Laboratory of Immunoregulation and Mucosal Immunology, Department of Molecular Biomedical Research, VIB, Technologiepark 927, 9052 Ghent, Belgium

Received 31 January 2013; Revised 15 March 2013; Accepted 16 March 2013

Academic Editor: Mohamad Mohty

Copyright © 2013 Anouk K. Gloudemans et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.