Abstract
Atopic dermatitis (AD) is a chronic inflammatory skin disorder, which often precedes food allergy, asthma, and allergic rhinitis-a progression known as the atopic march. A key feature of AD is elevated allergen-specific immunoglobulin E (IgE), indicating sensitization to environmental, microbial, and self-antigens. This study examines the mechanisms driving IgE sensitization in AD, including epidermal barrier dysfunction, immune dysregulation, antigen presentation, microbial imbalance, and genetic susceptibility. Understanding these pathways is essential for developing targeted therapies to prevent allergic disease progression and improve clinical outcomes.