ArticleThe Journal of investigative dermatology2013
Sensitization via healthy skin programs Th2 responses in individuals with atopic dermatitis.
Article in The Journal of investigative dermatology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 122 citations in OpenAlex.
- In Vitro Monitoring of Human T Cell Responses to Skin Sensitizing Chemicals-A Systematic Review.Cells · 2021Pooled it
- Food Avoidance Diets for Dermatitis.Current allergy and asthma reports · 2015Pooled it
- Reframing Eczema: Th2-Skewed Contact Sensitization, Atopy Patch Testing, and Systemic Contact Dermatitis.Current allergy and asthma reports · 2026Review
- Weak Sensitizers May Be Associated with CD80 Polymorphisms: Implications for Systemic Contact Dermatitis.JID innovations : skin science from molecules to population health · 2025Article
- Allergens in Atopic Dermatitis.Clinical reviews in allergy & immunology · 2025Review
- The immunobiology and therapeutic potential of regulatory T cells in autoimmune diseases and allergic diseases.Frontiers in immunology · 2025Review
- Spinal Calcrl+ neurons amplify mechanical itch signaling via synaptic plasticity in chronic itch model.PloS one · 2025Article
- Is Food-Triggered Atopic Dermatitis a Form of Systemic Contact Dermatitis?Clinical reviews in allergy & immunology · 2024Review
- Impaired expression of metallothioneins contributes to allergen-induced inflammation in patients with atopic dermatitis.Nature communications · 2023Article
- CTLA-4 suppresses hapten-induced contact hypersensitivity in atopic dermatitis model mice.Scientific reports · 2023Article
- Cutaneous dysbiosis may amplify barrier dysfunction in patients with atopic dermatitis.Frontiers in microbiology · 2022Article
- Advances in atopic dermatitis.Clinical medicine (London, England) · 2021Article
- Characterization of the Class I MHC Peptidome Resulting From DNCB Exposure of HaCaT Cells.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- Art of prevention: Allergic sensitization through damaged skin: Atopic, occupational, and stasis dermatitis.International journal of women's dermatology · 2020Review
- Article
- Disease Mechanisms in Atopic Dermatitis: A Review of Aetiological Factors.Acta dermato-venereologica · 2020Review
- Lipid depletion enables permeation ofTissue barriers · 2020Article
- Atopy patch tests may identify patients at risk for systemic contact dermatitis.Immunity, inflammation and disease · 2020Article
- Skin sensitization: Uncertainties, challenges, and opportunities for improved risk assessment.Contact dermatitis · 2019Article
- Contact Dermatitis in Atopic Dermatitis Children-Past, Present, and Future.Clinical reviews in allergy & immunology · 2019Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Allergen-specific responses in atopic dermatitis (AD) are skewed toward a Th2 profile. However, individuals with AD have been shown to make effective virus-specific Th1 responses, raising the possibility that the skin itself contributes to driving the AD Th2 immunophenotype. Therefore, to explore the programming of immunological sensitization by the skin, we examined the outcome of sensitization through non-lesional skin of individuals with AD and healthy controls. Volunteers (controls, AD individuals with filaggrin gene (FLG) mutations (ADFM), and AD individuals without FLG mutations (ADWT)) were sensitized by cutaneous application of 2,4-dinitrochlorobenzene (DNCB), a small, highly lipophilic chemical sensitizer. At the doses tested, DNCB showed equal penetration into skin of all groups. Clinical reactions to DNCB were significantly reduced in AD. Although both controls and AD made systemic DNCB-specific Th1 responses, these were reduced in AD and associated with significantly Th2-skewed DNCB-specific T-cell responses. Th2 skewing was seen in both ADFM and ADWT, with no difference between these groups. After 3 months, DNCB-specific Th2 responses were persistent in individuals with AD, and Th1 responses persisted in controls. These data provide evidence that when antigen penetration is not limiting, AD skin has a specific propensity to Th2 programming, suggesting the existence of altered skin immune signaling that is AD-specific and independent of FLG status.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.