What Causes Eczema?

Eczema, also known as atopic dermatitis, is a chronic, relapsing inflammatory skin disorder driven by a complex interplay of genetic predisposition, immune dysregulation, and environmental triggers. A key underlying factor is a compromised skin barrier—often due to loss-of-function mutations in the *FLG* gene encoding filaggrin, a structural protein critical for epidermal integrity. This defect increases transepidermal water loss and facilitates penetration of allergens, microbes, and irritants.

Immune dysfunction plays a central role: patients typically exhibit T-helper 2 (Th2) lymphocyte polarization, with elevated levels of interleukins IL-4, IL-13, and IL-31. These cytokines drive inflammation, pruritus, and epidermal hyperplasia. In chronic lesions, Th1 and Th17 pathways may also become activated, contributing to lichenification and tissue remodeling.

Environmental contributors—including exposure to soaps, detergents, wool or synthetic fabrics, airborne allergens (e.g., house dust mites, pollen), microbial colonization (notably *Staphylococcus aureus*), and psychological stress—can provoke or exacerbate flares. Importantly, while food allergies are commonly suspected, they are confirmed triggers in only a minority of cases—primarily in young children with moderate-to-severe disease—and should be evaluated only through evidence-based diagnostic protocols, not empiric elimination.