Cutaneous barrier dysfunction in allergic diseases
Open accessAbstract
The fundamental defect(s) that drives atopic dermatitis (AD) remains controversial. "Outside in" proponents point to the important association of filaggrin gene mutations and other skin barrier defects with AD. The "inside out" proponents derive support from evidence that AD occurs in genetic animal models with overexpression of type 2 immune pathways in their skin, and humans with gain-of-function mutations in their type 2 response develop severe AD. The observation that therapeutic biologics, targeting type 2 immune responses, can reverse AD provides compelling support for the importance of "inside out" mechanisms of AD. In this review, we propose a central role for epithelial cell dysfunction that accounts for the dual role of skin barrier defects and immune pathway activation in AD. The complexity of AD has its roots in the dysfunction of the epithelial barrier that allows the penetration of allergens, irritants, and microbes into a cutaneous milieu that facilitates the induction of type 2 immune responses. The AD phenotypes and endotypes that result in chronic skin inflammation and barrier dysfunction are modified by genes, innate/adaptive immune responses, and different environmental factors that cause skin barrier dysfunction. There is also compelling evidence that skin barrier dysfunction can alter the course of childhood asthma, food allergy, and allergic rhinosinusitis. Effective management of AD requires a multipronged approach, not only restoring cutaneous barrier function, microbial flora, and immune homeostasis but also enhancing skin epithelial differentiation.
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Epithelial barrier dysfunction induces type 2 immune responses and is considered an initial step in developing AD and the atopic march.
“Epithelial barrier dysfunction induces type 2 immune responses and is considered an initial step in developing atopic dermatitis (AD) and the atopic march (14, 16, 17).”
From Particulate matter causes skin barrier dysfunction. (2021) · cites this paper as [14]
A disrupted skin barrier promotes epicutaneous sensitization.
“Recently, it has been suggested that a disrupted skin barrier promotes epicutaneous sensitization (14, 16).”
From Particulate matter causes skin barrier dysfunction. (2021) · cites this paper as [14]
Skin barrier dysfunction is considered an initial step of the development of AD.
“In our current study, we focused on PM2.5-mediated skin barrier function directly because skin barrier dysfunction is considered an initial step of the development of AD (14, 19).”
From Particulate matter causes skin barrier dysfunction. (2021) · cites this paper as [14]
Maintaining normal skin barrier function is critical for the prevention and control of allergic diseases such as AD and food allergy.
“It has been suggested that maintaining normal skin barrier function is critical for the prevention and control of allergic diseases such as AD and food allergy (14, 16, 60–62).”
From Particulate matter causes skin barrier dysfunction. (2021) · cites this paper as [14]
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- Authors
- Leung, D. Y. M., Berdyshev, E., & Goleva, E.
- Affiliations
- National Jewish Health (US)
- Corresponding author
- Leung, Donald Y.M.
- Venue
- Journal of Allergy and Clinical Immunology
- Publisher
- Elsevier BV
- Published
- 2020-06
- Volume
- 145
- Issue
- 6
- Pages
- 1485-1497
- ISSN
- 0091-6749 (ISSN-L)
- PMC
- PMC7291847
- OpenAlex
- W3033163803
- Cited by
- 190
- References
- 139
- Citations by year
- 2026: 28 · 2025: 31 · 2024: 34 · 2023: 35 · 2022: 31 · 2021: 20 · 2020: 10 · 2019: 1
- FWCI
- 4.01
- Type
- journal article
- Language
- en
- Update notices
- erratum (2021-09-01)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Allergy and Clinical Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01 AR41256)
- NIH/National Institute of Allergy and Infectious Diseases (U19 AI117673)
- NIH/National Center for Research Resources (UL1 RR025780)
- National Jewish Health
- Topics
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Health Sciences › Medicine › Dermatology › Contact Dermatitis and Allergies
- Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
- Keywords
- atopic dermatitis, skin barrier dysfunction, filaggrin mutations, Th2 immune response, epithelial dysfunction, allergic diseases, childhood asthma, food allergy, allergic rhinosinusitis, skin microbiome, biologic therapy, skin inflammation
- MeSH terms
- Filaggrin Proteins, Allergens, Animals, Humans, Hypersensitivity, Immunity, Skin, Skin Diseases
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