ATOPIC dermatitis (AD), also known as atopic eczema, is the most common chronic inflammatory skin disease, affecting 10–20% of children and 2–10% of adults globally. The prevalence varies by region and population, with symptoms including dry, itchy, and inflamed skin. AD follows cycles of flare-ups and remissions, often triggered by stress, infections, weather changes, and allergens. While it typically begins in infancy, it can persist into adulthood, causing significant financial and psychological burdens on individuals and society.
AD arises from a complex interplay of genetic, immune, systemic, and environmental factors. Many patients have a family history of allergies such as asthma or rhinitis. Genetic mutations contribute to immune dysfunction and a weakened skin barrier, increasing susceptibility to irritation and infections. A deficiency in essential skin lipids leads to moisture loss, inflammation, and chronic itching, often resulting in skin thickening and lichenification. The immune response in AD is characterised by Th2 cell activation, IgE production, and cytokines such as IL-4, IL-5, and IL-13, which exacerbate inflammation and barrier dysfunction. While acute flares are largely Th2-driven, chronic AD involves Th1, Th17, and Th22 responses. Reduced antimicrobial peptides further weaken AD-affected skin, making it more vulnerable to infections, particularly by Staphylococcus aureus, which colonises up to 90% of patients and worsens the disease severity.
Current treatments focus on managing symptoms and include moisturisers, corticosteroids, calcineurin inhibitors, PDE4 inhibitors, phototherapy, immunomodulators, and biologics. However, the heterogeneity of AD has led researchers to define distinct endotypes—subgroups based on specific biological mechanisms. Advances in molecular profiling and immune characterisation have revealed significant variations across ethnicities, age groups, and disease severities. Emerging research suggests that multi-omics integration, including genomics, transcriptomics, and microbiome studies, could refine endotype classifications. By identifying specific immune pathways, scientists aim to develop personalised treatment approaches. Additionally, machine learning and artificial intelligence (AI) hold promise for predicting AD severity and treatment responses, paving the way for precision medicine in AD management.
Understanding AD endotypes is crucial for advancing personalised treatments tailored to individual genetic and molecular profiles. Continued research in multi-omics, long-term patient studies, and microbiome interactions will provide deeper insights into AD’s complexity. These advancements promise more effective and individualised treatments, improving outcomes for patients with this challenging condition.
Reference
Fyhrquist N et al. Endotypes of atopic dermatitis. J Allergy Clin Immunol. 2025;DOI:10.1016/j.jaci.2025.02.029.