Epicutaneous sensitization in the development of food allergy: what is the evidence and how can this be prevented?
Open accessAbstract
There is increasing evidence regarding the importance of allergic sensitization through the skin. In this review, we provide an overview of the atopic march and immune mechanism underlying the sensitization and effector phase of food allergy. We present experimental models and human data that support the concept of epicutaneous sensitization and how this forms one half of the dual‐allergen exposure hypothesis. We discuss specific important elements in the skin ( FLG and other skin barrier gene mutations, Langerhans cells, type 2 innate lymphoid cells, IL‐33, TSLP) that have important roles in the development of allergic responses as well as the body of evidence on environmental allergen exposure and how this can sensitize an individual. Given the link between skin barrier impairment, atopic dermatitis, food allergy, allergic asthma, and allergic rhinitis, it is logical that restoring the skin barrier and prevention or treating atopic dermatitis would have beneficial effects on prevention of related allergic diseases, particularly food allergy. We present the experimental and human studies that have evaluated this approach and discuss various factors which may influence the success of these approaches, such as the type of emollient chosen for the intervention, the role of managing skin inflammation, and differences between primary and secondary prevention of atopic dermatitis to achieve the desired outcome.
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The gastrointestinal route, mainly between the 4th and 6th months of life, is generally associated with induction of tolerance, with regulatory T and B cells playing a role.
“The gastrointestinal route, mainly in the interval between the 4th and 6th months of life, is generally associated with the induction of tolerance, as regulatory T and B cells have been described as playing a role in regulating the pathogenesis of AD and food allergy, as well as in the development of tolerance to the foods involved.”
From Update on the pathogenesis of atopic dermatitis. (2024) · cites this paper as [9]
The Pathogenesis of Food Allergy section (page unavailable) says early oral exposure causes tolerance, supporting the gastrointestinal-route part of the claim. The copy does not specify a 4th-to-6th-month interval or describe regulatory T and B cells as mediating that tolerance; they appear only in a reference title. The Limitations of Oral Tolerance Induction section instead describes a narrow window in early life without those details. (LLM, conf=0.87)
Experimental — accuracy not yet measuredSkin barrier dysfunction in AD increases permeability to allergens and irritants, contributing to loss of hydration and persistence of subclinical skin inflammation.
“The skin barrier dysfunction that occurs in AD increases permeability to allergens and irritants, contributing to loss of hydration and persistence of subclinical skin inflammation.”
From Update on the pathogenesis of atopic dermatitis. (2024) · cites this paper as [9]
The sections “Phenotypic Measure of Skin Barrier Dysfunction” and “Barrier Dysfunction and Its Role in AD and FA” state that impaired skin barriers allow greater water evaporation and penetration by allergens and irritants, and describe a cycle of inflammation and barrier disruption. The paper does not specifically establish that this process causes the persistence of subclinical skin inflammation. Page numbers were not provided in our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measuredThe main route for sensitization and perpetuation of food-induced hypersensitivity lesions is the cutaneous one.
“The main route for sensitization and perpetuation of food-induced hypersensitivity lesions is the cutaneous one.”
From Update on the pathogenesis of atopic dermatitis. (2024) · cites this paper as [9]
The In Vitro Measures of Epicutaneous Sensitization section says the findings suggest peanut sensitization can originate in the skin. The Identifying Skin Barrier Markers section says skin immune responses may contribute to the persistence or severity of food allergy. Neither section establishes the skin as the main route or specifically addresses the perpetuation of food-induced hypersensitivity lesions; page numbers were unavailable in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredFormation of subclinical inflammatory lesions and absorption of food antigens through the skin leads to sensitization in infants with AD.
“The formation of subclinical inflammatory lesions and the absorption of food antigens through the skin, whether due to contamination in dust or the use of products containing food proteins, leads to sensitization in infants with AD.”
From Update on the pathogenesis of atopic dermatitis. (2024) · cites this paper as [9]
The Environmental Exposure to Allergens in Humans section (page unavailable) links peanut sensitization in children with AD to environmental peanut dust and reports an association between peanut-containing skin creams and peanut allergy. The Barrier Dysfunction and Atopic March sections describe how impaired, inflamed skin may permit allergen exposure and sensitization. But the paper does not establish that *subclinical inflammatory lesions* form and cause sensitization in infants with AD; the human exposure evidence is largely observational, so the sentence states the mechanism more definitively than the source does. (LLM, conf=0.84)
Experimental — accuracy not yet measuredEpithelial 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 [16]
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 [16]
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 [16]
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Lack, G., & Golding, J. (1996) · BMJ · doi:10.1136/bmj.313.7052.300 · Cited by 25 · see citing works
Self-citationThe genetics of the skin barrier in eczema and other allergic disorders
Marenholz, I., Esparza-Gordillo, J., & Lee, Y. (2015) · Current Opinion in Allergy and Clinical Immunology · doi:10.1097/aci.0000000000000194 · Cited by 23 · see citing works
Vitamin D: can the sun stop the atopic epidemic?
Hawrylowicz, C. M., & Santos, A. F. (2019) · Current Opinion in Allergy and Clinical Immunology · doi:10.1097/aci.0000000000000613 · Cited by 23 · see citing works
Berents, T. L., Carlsen, K. C. L., Mowinckel, P., Skjerven, H. O., Rolfsjord, L. B., Bradley, M., Carlsen, K. ‐., & Gjersvik, P. J. (2016) · British Journal of Dermatology · doi:10.1111/bjd.15157 · Cited by 22 · see citing works
Pediatric food allergy-related household costs are influenced by age, but not disease severity
Wai, H. M., Middelveld, R. J. M., Thörnqvist, V., et al. (2019) · World Allergy Organization Journal · doi:10.1016/j.waojou.2019.100061 · Cited by 21 · see citing works
Distribution of peanut protein in school and home environments of inner-city children
Sheehan, W. J., Brough, H. A., Makinson, K., Petty, C. R., Lack, G., & Phipatanakul, W. (2017) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2017.05.042 · Cited by 19 · see citing works
Self-citationEvaluation of the epidemiology of peanut allergy in the United Kingdom
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Inhibition of the development of immediate hypersensitivity by staphylococcal enterotoxin B
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Self-citationThe value of oral immunotherapy
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Flagged first, then by citations
Research works printed but not linked: 2
- [127]Brough HAJ-L ZK; Logan K; Richards K; Perkin M; Peacock J; Flohr C; Lack G Early exposure to environmental peanut in dust is associated with the development of peanut allergy but this effect is abrogated by early peanut consumption In: European Asthma, Allergy and Clinical Immunology Annual Conference Munich, Germany; 2018.
- [171]Simpson EL, Chalmers JR, Hanifin JM, Thomas KS, Cork MJ, McLean WH, Emollient enhancement of the skin barrier from birth offers effective atopic dermatitis prevention. J Allergy Clin Immunol 2014; 134: 818– 823. 25282563 PMC4180007
Cited by
Sorted by citations
Particulate matter causes skin barrier dysfunction.
Kim, B. E., Kim, J., Goleva, E., Berdyshev, E., Lee, J., Vang, K. A., Lee, U. H., Han, S., Leung, S., Hall, C. F., et al. (2021) · JCI insight · doi:10.1172/jci.insight.145185 · Cited by 173 · see citing works
“dermatitis (AD) and the atopic march (14, 16, 17).”
BackgroundSelf-citationUpdate on the pathogenesis of atopic dermatitis.
Criado, P. R., Miot, H. A., Bueno-Filho, R., Ianhez, M., Criado, R. F. J., & de Castro, C. C. S. (2024) · Anais brasileiros de dermatologia · doi:10.1016/j.abd.2024.06.001 · Cited by 66 · see citing works
- Authors
- Brough, H. A., Nadeau, K. C., Sindher, S. B., Alkotob, S. S., Chan, S., Bahnson, H. T., Leung, D. Y. M., & Lack, G.
- Affiliations
- Guy's Hospital (GB)
- Stanford Medicine (US)
- Immune Tolerance Network (US)
- National Jewish Health (US)
- Corresponding author
- Brough, Helen A.
- ORCID
- Venue
- Allergy
- Publisher
- Wiley
- Published
- 2020-05-18
- Volume
- 75
- Issue
- 9
- Pages
- 2185-2205
- ISSN
- 0105-4538 (ISSN-L)
- 1398-9995
- PMC
- PMC7494573
- OpenAlex
- W3014726894
- Cited by
- 275
- References
- 173
- Citations by year
- 2026: 34 · 2025: 37 · 2024: 55 · 2023: 54 · 2022: 42 · 2021: 41 · 2020: 11
- FWCI
- 4.96
- Type
- journal article
- Language
- en
- Update notices
- correction (2026-03-24)
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Allergy (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Research Portal (King's College London) (submittedVersion, other-oa)
- Funders
- Sean N. Parker Center for Allergy and Asthma Research at Stanford University
- National Institutes of Health (R01AI140134, U19AI070535)
- Levin Foundation
- Reinhard Foundation
- Topics
- Health Sciences › Medicine › Immunology and Allergy › Food Allergy and Anaphylaxis Research
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Health Sciences › Medicine › Dermatology › Contact Dermatitis and Allergies
- Keywords
- epicutaneous sensitization, food allergy, atopic march, skin barrier, FLG gene mutations, Langerhans cells, ILC2, IL-33, thymic stromal lymphopoietin, atopic dermatitis, allergic asthma, allergic rhinitis, emollients, atopic dermatitis prevention, skin inflammation
- MeSH terms
- Filaggrin Proteins, Allergens, Dermatitis, Atopic, Food Hypersensitivity, Humans, Immunity, Innate, Lymphocytes
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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