Federica Trovato, Camilla Chello, S. Amato, Antonio Di Guardo, Emanuele AMORE, Luigi Bennardo, Antonio Giovanni Richetta, Teresa Grieco, Steven Paul Nisticò, Giovanni Pellacani, Annunziata Dattola
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.