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Key physiological features include: Filaggrin gene mutations , leading to a compromised skin barrier and increased transepidermal water loss Th2-skewed immune response , with elevated IL-4, IL-13, and IgE levels Colonization with Staphylococcus aureus , often contributing to inflammation and secondary infection Heightened mast cell activity , promoting pruritus and dermal reactivity This pathophysiology supports a dual treatment approach: barrier repair and inflammation modulation , often in combination with antimicrobial or immunosuppressive strategies