Airway responses towards allergens - from the airway epithelium to T cells

Dick Papazian, Søren Hansen, Peter A Würtzen

Research output: Contribution to journalReviewResearchpeer-review

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.

Original languageEnglish
JournalClinical and Experimental Allergy
Volume45
Issue number8
Pages (from-to)1268-1287
ISSN0954-7894
DOIs
Publication statusPublished - 2015

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Allergens
Epithelium
Th2 Cells
Environmental Exposure
Pathology
Population

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Papazian, Dick ; Hansen, Søren ; Würtzen, Peter A. / Airway responses towards allergens - from the airway epithelium to T cells. In: Clinical and Experimental Allergy. 2015 ; Vol. 45, No. 8. pp. 1268-1287.
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Airway responses towards allergens - from the airway epithelium to T cells. / Papazian, Dick; Hansen, Søren; Würtzen, Peter A.

In: Clinical and Experimental Allergy, Vol. 45, No. 8, 2015, p. 1268-1287.

Research output: Contribution to journalReviewResearchpeer-review

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AU - Papazian, Dick

AU - Hansen, Søren

AU - Würtzen, Peter A

N1 - This article is protected by copyright. All rights reserved.

PY - 2015

Y1 - 2015

N2 - 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.

AB - 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.

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