# From static pathology to dynamic immunity: immunological plasticity and histopathological remodeling in atopic dermatitis and psoriasis

**Authors:** Wei Shen, Yi Yao, Ying-Ming Ma, Xiao-Lei Xie, Shun-Li Tang, Yuan Wu, Hua-Jie Zhong, Yu-Mei Li, Hui Sun

PMC · DOI: 10.3389/fimmu.2026.1770896 · Frontiers in Immunology · 2026-02-13

## TL;DR

This paper explores how atopic dermatitis and psoriasis may be part of a continuous immune spectrum rather than distinct diseases, emphasizing the need for dynamic immune profiling in diagnosis.

## Contribution

The paper proposes that AD and psoriasis represent a spectrum linked by immune plasticity, challenging traditional histopathological classifications.

## Key findings

- Clinical observations show mixed immunophenotypes in AD and overlap syndromes.
- Immune cell plasticity and crosstalk with the microenvironment drive disease heterogeneity.
- Dynamic immunopathological profiling is suggested to improve precision medicine approaches.

## Abstract

Atopic dermatitis (AD) and psoriasis are the two canonical chronic inflammatory skin disorders, classically differentiated by their distinct histopathological features and immune polarization—Th2-dominant in AD versus IL-23/Th17-dominant in psoriasis. However, this conventional dichotomy is increasingly contested by clinical observations, such as the mixed immunophenotypes seen in Asian AD and overlap syndromes, which complicate clear-cut classification. Growing evidence highlights substantial immunological plasticity and pathological overlap, suggesting that these diseases may represent segments of a continuous spectrum rather than discrete entities. In this Mini Review, we integrate classical morphological observations with recent advances in molecular immunology to explore the mechanisms underlying these tissue responses. We examine how immune cell plasticity—particularly of tissue-resident memory T cells—and their crosstalk with the structural microenvironment contribute to disease heterogeneity and therapy-induced phenotypic shifts. We propose that a shift from static histologic evaluation toward dynamic immunopathological profiling is crucial for narrowing the gap between conventional diagnosis and the emerging paradigm of precision medicine.

## Linked entities

- **Diseases:** atopic dermatitis (MONDO:0004980), psoriasis (MONDO:0005083)

## Full-text entities

- **Genes:** IL25 (interleukin 25) [NCBI Gene 64806] {aka IL17E}, IL33 (interleukin 33) [NCBI Gene 90865] {aka C9orf26, DVS27, IL1F11, NF-HEV, NFEHEV}, IL22 (interleukin 22) [NCBI Gene 50616] {aka IL-21, IL-22, IL-D110, IL-TIF, ILTIF, TIFIL-23}, GATA3 (GATA binding protein 3) [NCBI Gene 2625] {aka HDR, HDRS}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, IGHE (immunoglobulin heavy constant epsilon) [NCBI Gene 3497] {aka IgE}, FLG (filaggrin) [NCBI Gene 2312] {aka ATOD2, FLG-1, FLG1}, IL17F (interleukin 17F) [NCBI Gene 112744] {aka CANDF6, IL-17F, ML-1, ML1}, IL5 (interleukin 5) [NCBI Gene 3567] {aka EDF, IL-5, TRF}, IL13 (interleukin 13) [NCBI Gene 3596] {aka IL-13, P600}, IFNG (interferon gamma) [NCBI Gene 3458] {aka IFG, IFI, IMD69}, IL4 (interleukin 4) [NCBI Gene 3565] {aka BCGF-1, BCGF1, BSF-1, BSF1, IL-4}, TSLP (thymic stromal lymphopoietin) [NCBI Gene 85480], IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, IL23A (interleukin 23 subunit alpha) [NCBI Gene 51561] {aka IL-23, IL-23A, IL23P19, P19, SGRF}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, IL4R (interleukin 4 receptor) [NCBI Gene 3566] {aka CD124, IL-4RA, IL4RA}
- **Diseases:** bleeding (MESH:D006470), spongiotic dermatitis (MESH:D003872), PsO (MESH:D011565), Psoriasiform dermatitis (OMIM:616834), acanthosis (MESH:D000052), fibrosis (MESH:D005355), cutaneous inflammation (MESH:D007249), Chronic inflammatory skin diseases (MESH:D012871), systemic inflammatory disease (MESH:D018746), hyperkeratosis (MESH:D017488), edema (MESH:D004487), parakeratosis (MESH:D010241), epidermal hyperplasia (MESH:D006965), AD (MESH:D003876), immune dysregulation (OMIM:614878), rheumatoid arthritis (MESH:D001172), X (MESH:D000326), Crohn's disease (MESH:D003424), infection (MESH:D007239), eruptions (MESH:D003875)
- **Chemicals:** lipid (MESH:D008055), dupilumab (MESH:C582203)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12945763/full.md

## References

100 references — full list in the complete paper: https://tomesphere.com/paper/PMC12945763/full.md

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Source: https://tomesphere.com/paper/PMC12945763