What causes eczema?

Eczema, also known as atopic dermatitis, is a chronic, relapsing inflammatory skin disorder resulting from a complex interplay of genetic, immunologic, and environmental factors. A primary underlying cause is a dysfunction in the skin barrier—often linked to loss-of-function mutations in the *FLG* gene encoding filaggrin, a key structural protein essential for epidermal integrity and hydration. This compromised barrier allows increased transepidermal water loss and facilitates penetration of allergens, irritants, and microbes, triggering immune activation.

Immunologically, eczema involves a dysregulated T-helper 2 (Th2) immune response, characterized by elevated levels of interleukins IL-4, IL-13, and IL-31, which drive inflammation, pruritus (itching), and further barrier disruption. In chronic lesions, Th1 and Th17 pathways may also become involved, contributing to lichenification and persistent inflammation.

Environmental triggers—including dry air, harsh soaps, wool or synthetic fabrics, sweat, pollen, dust mites, and certain foods (particularly in infants and young children with comorbid food allergy)—can provoke or exacerbate flares. Psychological stress and skin infections (e.g., *Staphylococcus aureus* colonization) are also well-documented contributors to disease activity and severity.

It is important to recognize that eczema is not caused by poor hygiene or contagious agents; rather, it reflects an inherited predisposition interacting with modifiable external factors. Accurate diagnosis and individualized management—including emollient therapy, topical anti-inflammatory agents (e.g., corticosteroids or calcineurin inhibitors), trigger avoidance, and, when indicated, systemic biologics such as dupilumab—form the cornerstone of effective long-term care.