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Peer-reviewedCC BY-NCDermatology practical & conceptual

Shared Pathways between Psoriasis and Atopic Dermatitis.

  1. 1Dermatology Unit, Istituto Dermopatico dell'Immacolata IDI-IRCCS, Rome, Italy.
  2. 2Dermatology Unit, Department of Medical and Cardiovascular Sciences, La Sapienza University of Rome, Rome, Italy.

Abstract

Introduction

Psoriasis and atopic dermatitis are leading examples of chronic inflammatory dermatoses with distinct clinical manifestations, pathogenesis, and demographic patterns. However, recent research has revealed overlapping immunological pathways that could serve as promising therapeutic targets.Objectives

To synthesize the principal immunological, epidermal barrier, and microbiome pathways shared by psoriasis and atopic dermatitis and to discuss their potential translational and therapeutic implications.Methods

We conducted a narrative review of the literature on PubMed from January 2000 to June 2024, using keywords such as "psoriasis," "atopic dermatitis," "cytokine pathways," "T cells," and "environmental triggers." Studies were selected based on their relevance to shared mechanisms between these diseases, focusing on cytokine profiles, immune cell activity, and skin barrier dysfunction.Results

Our review identified significant overlaps in cytokine-mediated pathways, particularly the IL-17/IL-22 axis, which mediates keratinocyte hyperproliferation and inflammation in both diseases. T cell dysregulation, including Th17 and Th22 activity, plays a pivotal role in maintaining chronic inflammation. Both conditions also exhibit impaired skin barrier function, linked to filaggrin loss-of-function mutations in atopic dermatitis and abnormal keratinocyte differentiation in psoriasis.Conclusion

These findings suggest that targeting shared mechanisms, such as the Th17 and Th22 pathways, along with barrier repair strategies may enable dual therapeutic benefits. This review underscores the potential for integrative treatment approaches and personalized medicine in managing chronic inflammatory skin disorders.

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BibTeX
@article{trovato2026shared,
  title = {{Shared Pathways between Psoriasis and Atopic Dermatitis.}},
  author = {Federica Trovato and Camilla Chello and Simone Amato and Antonio Di Guardo and Emanuele Amore and Luigi Bennardo and Antonio Giovanni Richetta and Teresa Grieco and Steven Paul Nisticò and Giovanni Pellacani and Annunziata Dattola},
  journal = {Dermatology practical \& conceptual},
  year = {2026},
  month = jul,
  doi = {10.5826/dpc.1603a6662},
  url = {https://europepmc.org/article/MED/42858415},
  note = {CC BY-NC},
}
RIS
TY  - JOUR
TI  - Shared Pathways between Psoriasis and Atopic Dermatitis.
AU  - Federica Trovato
AU  - Camilla Chello
AU  - Simone Amato
AU  - Antonio Di Guardo
AU  - Emanuele Amore
AU  - Luigi Bennardo
AU  - Antonio Giovanni Richetta
AU  - Teresa Grieco
AU  - Steven Paul Nisticò
AU  - Giovanni Pellacani
AU  - Annunziata Dattola
PY  - 2026
DA  - 2026/07/31
JO  - Dermatology practical & conceptual
DO  - 10.5826/dpc.1603a6662
UR  - https://europepmc.org/article/MED/42858415
AB  - Introduction  Psoriasis and atopic dermatitis are leading examples of chronic inflammatory dermatoses with distinct clinical manifestations, pathogenesis, and demographic patterns. However, recent research has revealed overlapping immunological pathways that could serve as promising therapeutic targets.Objectives  To synthesize the principal immunological, epidermal barrier, and microbiome pathways shared by psoriasis and atopic dermatitis and to discuss their potential translational and therapeutic implications.Methods  We conducted a narrative review of the literature on PubMed from January 2000 to June 2024, using keywords such as "psoriasis," "atopic dermatitis," "cytokine pathways," "T cells," and "environmental triggers." Studies were selected based on their relevance to shared mechanisms between these diseases, focusing on cytokine profiles, immune cell activity, and skin barrier dysfunction.Results  Our review identified significant overlaps in cytokine-mediated pathways, particularly the IL-17/IL-22 axis, which mediates keratinocyte hyperproliferation and inflammation in both diseases. T cell dysregulation, including Th17 and Th22 activity, plays a pivotal role in maintaining chronic inflammation. Both conditions also exhibit impaired skin barrier function, linked to filaggrin loss-of-function mutations in atopic dermatitis and abnormal keratinocyte differentiation in psoriasis.Conclusion  These findings suggest that targeting shared mechanisms, such as the Th17 and Th22 pathways, along with barrier repair strategies may enable dual therapeutic benefits. This review underscores the potential for integrative treatment approaches and personalized medicine in managing chronic inflammatory skin disorders.
SN  - 2160-9381
ER  -