The role of type 2 inflammation in the pathogenesis of atopic dermatitis

Relevance. Atopic dermatitis (AD) is classified as a chronic immune-­mediated disease, with its pathogenesis rooted in genetic predisposition and immune response dysregulation, predominantly driven by T2‑inflammatory reactions. This review highlights key aspects of the immunopathogenesis of AD, emphasizing its systemic inflammatory nature linked to T2‑immune dysregulation. This leads to the activation of cytokines such as IL‑4, IL‑5, IL‑13, and IL‑31. The article analyzes modern treatment approaches, including targeted therapy aimed at blocking T2 cytokines, stressing the importance of early intervention to prevent complications and the development of the atopic march. Understanding T2‑inflammation mechanisms opens new opportunities for developing effective personalized therapies for AD. Conclusion. Type 2 inflammation plays a pivotal role in the pathogenesis of AD, driving chronic inflammation, skin barrier dysfunction, and the clinical manifestations of the disease. Key mediators of T2 inflammation-­including IL‑4, IL‑5, IL‑13, and IL‑31‑regulate the activation of various immune-­competent cells, not only amplifying inflammation but also contributing to the development of pruritus. This, in turn, establishes the self-perpetuating “itch-scratch” cycle, which exacerbates skin damage and further stimulates inflammatory processes. Impaired skin barrier function also facilitates the penetration of allergens and microbial agents, further activating the immune response and worsening disease severity. Studying type 2 inflammation as a central mechanism in AD pathogenesis not only advances our understanding of the disease but also facilitates the development of new therapeutic strategies to control AD and improve patients’ quality of life, which remains a priority in contemporary immunology, allergology, and dermatology.