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This article has been retracted as it was found to contain a substantial amount of material from the following published article: “Allergic bronchopulmonary aspergillosis in asthma and cystic fibrosis” published in Clinical and Developmental Immunology, vol. 2011, Article ID 843763, 13 pages, 2011, DOI: 10.1155/2011/843763.

View the full Retraction here.


  1. A. P. Knutsen, “Immunopathology and immunogenetics of allergic bronchopulmonary aspergillosis,” Journal of Allergy, vol. 2011, Article ID 785983, 9 pages, 2011.
Journal of Allergy
Volume 2011, Article ID 785983, 9 pages
Review Article

Immunopathology and Immunogenetics of Allergic Bronchopulmonary Aspergillosis

Departments of Pediatrics, Division of Allergy and Immunology, Saint Louis University, 1465 S. Grand Boulevard, St. Louis, MO 63104, USA

Received 3 May 2011; Accepted 14 July 2011

Academic Editor: Prescott Woodruff

Copyright © 2011 Alan P. Knutsen. 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 bronchopulmonary aspergillosis (ABPA) is a Th2 hypersensitivity lung disease in response to Aspergillus fumigatus that affects asthmatic and cystic fibrosis (CF) patients. Sensitization to A. fumigatus is common in both atopic asthmatic and CF patients, yet only 1%–2% of asthmatic and 7%–9% of CF patients develop ABPA. ABPA is characterized by wheezing and pulmonary infiltrates which may lead to pulmonary fibrosis and/or bronchiectasis. The inflammatory response is characterized by Th2 responses to Aspergillus allergens, increased serum IgE, and eosinophilia. A number of genetic risks have recently been identified in the development of ABPA. These include HLA-DR and HLA-DQ, IL-4 receptor alpha chain (IL-4RA) polymorphisms, IL-10 −1082GA promoter polymorphisms, surfactant protein A2 (SP-A2) polymorphisms, and cystic fibrosis transmembrane conductance regulator gene (CFTR) mutations. The studies indicate that ABPA patients are genetically at risk to develop skewed and heightened Th2 responses to A. fumigatus antigens. These genetic risk studies and their consequences of elevated biologic markers may aid in identifying asthmatic and CF patients who are at risk to the development of ABPA. Furthermore, these studies suggest that immune modulation with medications such as anti-IgE, anti-IL-4, and/or IL-13 monoclonal antibodies may be helpful in the treatment of ABPA.