- Authors:
- DOI:
- 10.1111/cea.12451
- Abstract:
- The prevalence of allergic diseases such as allergic rhinitis is increasing, affecting up to 30% of the human population worldwide. Allergic sensitization arises from complex interactions between environmental exposures and genetic susceptibility, resulting in inflammatory T helper 2 (Th2) cell derived immune responses towards environmental allergens. Emerging evidence now suggest that an epithelial dysfunction, coupled with inherent properties of environmental allergens, can be responsible for the inflammatory responses towards allergens. Several epithelial derived cytokines, such as thymic stromal lymphopoietin (TSLP), IL-25 and IL-33 influence tissue-resident dendritic cells (DCs) as well as Th2 effector cells. Exposure to environmental allergens does not elicit Th2 inflammatory responses or any clinical symptoms in non-atopic individuals and recent findings suggest that a non-damaged, healthy epithelium lowers the DCs ability to induce inflammatory T cell responses towards allergens. The purpose of this review is to summarize the current knowledge on which signals from the airway epithelium, from first contact with inhaled allergens all the way to the ensuing Th2 cell responses, influence the pathology of allergic diseases. This article is protected by copyright. All rights reserved.
- Type:
- Journal review article
- Language:
- English
- Published in:
- Clinical and Experimental Allergy, 2015, Vol 45, Issue 8, p. 1268-1287
- Main Research Area:
- Medical science
- Publication Status:
- Published
- Review type:
- Peer Review
- Submission year:
- 2015
- Scientific Level:
- Scientific
- ID:
- 2260777065