Pathogenesis and management of atopic dermatitis: insights into epidermal barrier dysfunction and immune mechanisms

Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by a compromised epidermal barrier and heightened immunoglobulin E (IgE) levels, often associated with filaggrin (FLG) gene mutations. Genetic factors like FLG mutations and environmental influences, including microbial exposure and pollutants, contribute to the disease’s progression, leading to itchy, inflamed skin. AD frequently coexists with allergic conditions, severely affecting the quality of life. The disease’s pathogenesis involves complex interactions between genetic predispositions, immune responses, and environmental triggers. Despite advances, the development of effective treatments remains challenging due to an incomplete understanding of how FLG mutations influence immune pathways and the variability in AD presentation. Current biomarkers are insufficient to fully capture disease complexity or predict therapeutic responses, highlighting the need for novel biomarkers and personalized approaches. Emerging therapies such as chimeric antigen receptor (CAR)-T cell therapy, stem cell therapy, and regenerative medicine show promise in addressing AD’s root causes. This review explores key aspects of AD pathogenesis, focusing on epidermal barrier dysfunction, immune mechanisms, and the need for innovative therapeutic strategies to improve patient outcomes.