Atopic eczema is a chronic, relapsing, inflammatory skin condition characterized by itch which affects 20–30% of schoolchildren and 5–10% of adults in the UK. The increased prevalence in both western industrialized countries and developing nations over the last 20 years highlights the strong role of environmental factors in mediating the disease. However, the identification of a strong association between atopic eczema and mutations in the gene encoding filaggrin in 2006 has provided a paradigm shift in our understanding of the role of genetics in this condition and the importance of the function of the epidermal barrier. Indeed, interventions to repair the epidermal barrier show promise in both the treatment and prevention of atopic eczema and its complications. T‐helper 2 cells are central to mediating atopic eczema inflammation and specific targeted interventions are progressing well in clinical trials. Further developments in our understanding of disease pathogenesis, including the role of thymic stromal lymphopoeitin, and recently discovered subsets of immunocytes, are exciting targets and provide an optimistic future for the management of this challenging disease. However, topical therapy with emollients, corticosteroids and calcineurin inhibitors remains the mainstay of treatment. Thus, for more severe disease, current therapeutic options remain limited. As a result, atopic eczema still contributes a significant quality of life and financial burden on society and health care systems worldwide.

Keywords eczema, atopic, filaggrin, skin barrier, Staphylococcus aureus, herpes simplex, immunosuppression