Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disorder characterized by intense pruritus, eczematous lesions, and impaired skin barrier function. The pathogenesis of AD involves a complex interplay between genetic predisposition, immune dysregulation, and environmental triggers. Filaggrin gene mutations and other skin barrier defects facilitate allergen penetration and microbial colonization, while acute lesions are typically dominated by Th2-mediated immune responses and chronic lesions show a mixed Th1/Th2/Th17 profile. Environmental factors, including allergens and microbial colonization, exacerbate disease activity and contribute to flare-ups. Management strategies involve skin barrier restoration, topical and systemic anti-inflammatory therapies, and targeted biologics such as dupilumab. Understanding the immunopathogenesis of AD is essential for optimizing clinical management and improving patient outcomes. This review summarizes current evidence on genetic, immunological, and environmental factors contributing to AD and highlights contemporary approaches to effective clinical care.

Atopic dermatitis; Immunopathogenesis; Skin barrier dysfunction; Th2 cytokines; Chronic inflammation; Clinical management; Biologic therapy

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