Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2017 Jul;278(1):116-130.
doi: 10.1111/imr.12546.

The atopic march: current insights into skin barrier dysfunction and epithelial cell-derived cytokines

Hongwei Han  1 , Florence Roan  1 , Steven F Ziegler  1   2
Affiliations
Review

The atopic march: current insights into skin barrier dysfunction and epithelial cell-derived cytokines

Hongwei Han et al. Immunol Rev. 2017 Jul.

Abstract

Atopic dermatitis often precedes the development of other atopic diseases. The atopic march describes this temporal relationship in the natural history of atopic diseases. Although the pathophysiological mechanisms that underlie this relationship are poorly understood, epidemiological and genetic data have suggested that the skin might be an important route of sensitization to allergens. Animal models have begun to elucidate how skin barrier defects can lead to systemic allergen sensitization. Emerging data now suggest that epithelial cell-derived cytokines such as thymic stromal lymphopoietin (TSLP), IL-33, and IL-25 may drive the progression from atopic dermatitis to asthma and food allergy. This review focuses on current concepts of the role of skin barrier defects and epithelial cell-derived cytokines in the initiation and maintenance of allergic inflammation and the atopic march.

Keywords: TSLP; IL-33; allergic; atopic; epithelial; inflammation.

PubMed Disclaimer

Conflict of interest statement

Conflict of Interest: H.H., F.R., and S.F.Z. declare no financial or commercial conflict of interest.

Figures

Figure 1
Figure 1. A model of barrier disruption and skin sensitization
Allergens, infections, and tissue damage can all stimulate release of TSLP, IL-33, and IL-25 from the epithelium. These epithelial cell-derived cytokines license DCs to drive type 2 responses but also act on a variety of cell types, including basophils, eosinophils, mast cells and ILCs to initiate and maintain allergic inflammation.
See this image and copyright information in PMC

References

    1. Coca AF, Cooke RA. On the Classification of the Phenomena of Hypersensitiveness. J Immunol. 1923;8:163–182.
    1. Wahn U. What drives the allergic march? Allergy. 2000;55:591–599. - PubMed
    1. Rhodes HL, Sporik R, Thomas P, Holgate ST, Cogswell JJ. Early life risk factors for adult asthma: a birth cohort study of subjects at risk. J Allergy Clin Immunol. 2001;108:720–725. - PubMed
    1. Rhodes HL, Thomas P, Sporik R, Holgate ST, Cogswell JJ. A birth cohort study of subjects at risk of atopy: twenty-two-year follow-up of wheeze and atopic status. Am J Respir Crit Care Med. 2002;165:176–180. - PubMed
    1. Burks AW, Tang M, Sicherer S, et al. ICON: food allergy. J Allergy Clin Immunol. 2012;129:906–920. - PubMed

Publication types