Intrinsic atopic dermatitis shows similar TH2 and higher TH17 immune activation compared with extrinsic atopic dermatitis
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Background Atopic dermatitis (AD) is classified as extrinsic and intrinsic, representing approximately 80% and 20% of patients with the disease, respectively. Although sharing a similar clinical phenotype, only extrinsic AD is characterized by high serum IgE levels. Because most patients with AD exhibit high IgE levels, an "allergic"/IgE-mediated disease pathogenesis was hypothesized. However, current models associate AD with T-cell activation, particularly TH2/TH22 polarization, and epidermal barrier defects.Objective We sought to define whether both variants share a common pathogenesis.Methods We stratified 51 patients with severe AD into extrinsic AD (n = 42) and intrinsic AD (n = 9) groups (with similar mean disease activity/SCORAD scores) and analyzed the molecular and cellular skin pathology of lesional and nonlesional intrinsic AD and extrinsic AD by using gene expression (real-time PCR) and immunohistochemistry.Results A significant correlation between IgE levels and SCORAD scores (r = 0.76, P < 10(-5)) was found only in patients with extrinsic AD. Marked infiltrates of T cells and dendritic cells and corresponding epidermal alterations (keratin 16, Mki67, and S100A7/A8/A9) defined lesional skin of patients with both variants. However, higher activation of all inflammatory axes (including TH2) was detected in patients with intrinsic AD, particularly TH17 and TH22 cytokines. Positive correlations between TH17-related molecules and SCORAD scores were only found in patients with intrinsic AD, whereas only patients with extrinsic AD showed positive correlations between SCORAD scores and TH2 cytokine (IL-4 and IL-5) levels and negative correlations with differentiation products (loricrin and periplakin).Conclusions Although differences in TH17 and TH22 activation exist between patients with intrinsic AD and those with extrinsic AD, we identified common disease-defining features of T-cell activation, production of polarized cytokines, and keratinocyte responses to immune products. Our data indicate that a TH2 bias is not the sole cause of high IgE levels in patients with extrinsic AD, with important implications for similar therapeutic interventions.
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IgE responses against environmental allergens and self proteins correlate with cutaneous inflammation and overall AD severity.
“A significant part of the sensitization process leading to the generation of IgE responses against environmental allergens (including food allergens)100 as well as against self proteins101 correlates with cutaneous inflammation and overall severity102,103.”
From Atopic dermatitis: an expanding therapeutic pipeline for a complex disease (2022) · cites this paper as [103]
The Results (page unavailable) report that total IgE levels correlated with AD severity measured by SCORAD in extrinsic AD, but not intrinsic AD. The Discussion (page unavailable) considers a possible effect of IgE on skin inflammation; it does not establish that effect or show that IgE responses to environmental allergens or self proteins correlate with inflammation or severity. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThere is increasing evidence that the IL-23-IL-17 axis and IL-36 may have a role in some AD subtypes, such as the intrinsic form and in Asian patients.
“there is increasing evidence that the IL-23–IL-17 axis as well as IL-36 (see above) may have a role, at least in some AD subtypes such as the so-called intrinsic form and in Asian patients73,103,117,123–125.”
From Atopic dermatitis: an expanding therapeutic pipeline for a complex disease (2022) · cites this paper as [103]
The Results and Discussion report stronger IL-17/Th17 and IL-23-related activity in intrinsic than extrinsic atopic dermatitis, supporting a possible role for that axis in the intrinsic subtype. The paper mentions IL-36 only in discussing a proposed mechanism drawn from psoriasis research; it does not establish a role for IL-36 in atopic dermatitis or address Asian patients. Page numbers were not available in our copy. (LLM, conf=0.88)
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Simpson, E. L., Imafuku, S., Poulin, Y., Ungar, B., Zhou, L., Malik, K., Wen, H.-C., Xu, H., Estrada, Y. D., Peng, X., et al. (2019) · Journal of Investigative Dermatology · doi:10.1016/j.jid.2018.10.043 · Cited by 120 · see citing works
Self-citationAmat, F., Soria, A., Tallon, P., Bourgoin‐Heck, M., Lambert, N., Deschildre, A., & Just, J. (2018) · Clinical & Experimental Allergy · doi:10.1111/cea.13156 · Cited by 73 · see citing works
Bernard, M., Carrasco, C., Laoubi, L., Guiraud, B., Rozières, A., Goujon, C., Duplan, H., Bessou‐Touya, S., Nicolas, J., Vocanson, M., et al. (2017) · The Journal of Pathology · doi:10.1002/path.4887 · Cited by 66 · see citing works
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<scp>CLA</scp><sup>+</sup> memory T cells in atopic dermatitis: CLA+ T cells and atopic dermatitis
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- Authors
- Suárez-Fariñas, M., Dhingra, N., Gittler, J., Shemer, A., Cardinale, I., de Guzman Strong, C., Krueger, J. G., & Guttman-Yassky, E.
- Affiliations
- Columbia University (US)
- Albert Einstein College of Medicine (US)
- Rockefeller University (US)
- Venue
- Journal of Allergy and Clinical Immunology
- Publisher
- Elsevier BV
- Published
- 2013-08
- Volume
- 132
- Issue
- 2
- Pages
- 361-370
- ISSN
- 0091-6749 (ISSN-L)
- PMC
- PMC3991240
- OpenAlex
- W2003774999
- Cited by
- 483
- References
- 63
- Citations by year
- 2026: 30 · 2025: 24 · 2024: 40 · 2023: 39 · 2022: 41 · 2021: 51 · 2020: 42 · 2019: 35 · 2018: 36 · 2017: 48 · 2016: 37 · 2015: 29 · 2014: 25 · 2013: 5
- FWCI
- 37.01
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Allergy and Clinical Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Center for Research Resources (UL1RR024143)
- Topics
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Health Sciences › Medicine › Dermatology › Contact Dermatitis and Allergies
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Keywords
- atopic dermatitis, intrinsic atopic dermatitis, extrinsic atopic dermatitis, Th17 cells, Th22 cells, Th2 cytokines, serum IgE, T cell activation, keratinocyte differentiation, skin barrier, IL-4, IL-5, SCORAD, pathogenesis
- MeSH terms
- Filaggrin Proteins, Adult, Aged, Dermatitis, Atopic, Female, Humans, Immunoglobulin E, Inflammation, Lymphocyte Activation, Male, Middle Aged, Skin, Keratinocytes, Cytokines, Th2 Cells, Young Adult, Th17 Cells
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