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Epithelial Barrier Dysfunction in Atopic Dermatitis, Allergic Contact Dermatitis, and Chronic Spontaneous Urticaria and its Therapeutic Implications
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DOI：10.1007/s11882-026-01275-4.png)
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Abstract
En 中文
Allergic skin diseases arise from complex interactions between epithelial barrier dysfunction and immune dysregulation. This review examines how structural and functional defects in the epidermal barrier predispose to conditions such as atopic dermatitis, allergic contact dermatitis, and chronic spontaneous urticaria, and explores how mechanistic insights into these abnormalities guide therapeutic selection. Advances in molecular and genetic research have clarified the roles of filaggrin deficiency, lipid disorganization, altered skin pH, tight junction impairment, antimicrobial peptide imbalance, and microbiome disruption in driving barrier vulnerability and downstream immune activation. Parallel progress in immunology has identified key signaling pathways including JAK-STAT, IL-4/IL-13, OX40, BTK, and KIT that sustain inflammation and disease chronicity. These discoveries have led to the expansion of biologic and small-molecule therapies, with additional agents targeting barrier restoration and immune memory currently in development. Identification of specific epithelial and immune defects has provided a unifying framework for understanding susceptibility, chronicity, and relapse across allergic skin diseases. Ongoing research focused on epidermal barrier biology, microbiome modulation, and translational immunology has the potential to refine therapeutic selection, improve long-term disease control, and guide future drug development.
Keywords:
Allergic contact dermatitis
Allergic skin disease
Atopic dermatitis
Chronic spontaneous urticaria
Epithelial barrier
Filaggrin
Inflammation
Therapeutic implications
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