Immunological pathomechanisms of spongiotic dermatitis in skin lesions of atopic dermatitis
Open accessAbstract
Atopic dermatitis (AD) is a chronic pruritic skin disease with a complex pathogenesis underlying its heterogeneous clinical phenotypes and endotypes. The skin manifestation of AD reflects the cytokine milieu of a type-2-dominant immunity axis induced by genetic predisposition, innate immunity dysregulation, epidermal barrier defects, and allergic inflammation. However, the detailed pathomechanism of eczematous dermatitis, which is the principal characteristic of AD, remains unclear. This review examines previous studies demonstrating research progress in this area and considers the immunological pathomechanism of “spongiotic dermatitis”, which is the histopathological hallmark of eczematous dermatitis. Studies in this field have revealed the importance of IgE-mediated delayed-type hypersensitivity, the Fas/Fas-ligand system, and cell-mediated cytotoxicity in inducing the apoptosis of keratinocytes in spongiotic dermatitis. Recent studies have demonstrated that, together with infiltrating CD4 T cells, IgE-expressing dendritic cells (i.e., inflammatory dendritic epidermal cells and Langerhans cells) that capture specific allergens (i.e., house dust mites) are present in the spongiotic epidermis of lichenified eczema in patients with IgE-allergic AD. These findings suggest that IgE-mediated delayed-type hypersensitivity plays a pivotal role in the pathogenesis of spongiotic dermatitis in the skin lesions of AD.
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The presence of IgEs specific to certain allergens plays a role in the development of eczematous dermatitis resulting from IgE-mediated delayed-type hypersensitivity, functioning primarily as an amplifier of other factors involved in the pathogenesis of AD.
“However, the presence of IgEs specific to certain allergens plays a role in the development of eczematous dermatitis resulting from IgE-mediated delayed-type hypersensitivity, functioning primarily as an amplifier of other factors involved in the pathogenesis of AD.79, 80”
From Update on the pathogenesis of atopic dermatitis. (2024) · cites this paper as [79]
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Cited by
Sorted by citations
Update 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
- Tanei, R., & Hasegawa, Y.
- Affiliations
- Tokyo Metropolitan Institute of Gerontology (JP)
- Corresponding author
- Tanei, Ryoji
- ORCID
- Tanei, Ryoji
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2022-06-15
- Volume
- 23
- Issue
- 12
- Pages
- 6682
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC9223609
- OpenAlex
- W4282980032
- Cited by
- 33
- References
- 5
- Citations by year
- 2026: 8 · 2025: 11 · 2024: 6 · 2023: 6 · 2022: 2
- FWCI
- 1.11
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- 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, spongiotic dermatitis, eczematous dermatitis, Fas/Fas ligand, keratinocyte apoptosis, dendritic epidermal T cells, Langerhans cells, house dust mite allergy, Th2 immune response, CD4+ T cells, skin barrier dysfunction, allergic inflammation
- MeSH terms
- Allergens, Chronic Disease, Dermatitis, Atopic, Eczema, Humans, Hypersensitivity, Immunoglobulin E
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