Atopic dermatitis (AtD) is a common chronic dermatosis of multifactorial nature with prevalence of genetic component and complex pathogenesis. AtD manifestation usually starts from an infancy or early childhood; it may affect 15—25% of all children, but a considerable amount of patients resolves with age. 7—10% of adult population are susceptible to AtD. This disease is characterized by a severe itch, recurring eczematous lesions and intermittent course. Several pathophysiological mechanisms contribute to AtD clinical manifestations. For example, an impairment of epidermal barrier function, due to the deficiency of the structural protein filaggrin, can promote inflammation and T-cell infiltration. There is a polarization of an immune response in case of AtD in Th2-way, thus may lead to an epidermal barrier disruption. Other contributing factors to AtD onset include dysbiosis of the skin microbiota (in particular overgrowth of Staphylococcus aureus), systemic immune responses (including immunoglobulin E — mediated sensitization). Over time, the pathogenesis concept of this disease has undergone significant changes. This article provides an up-to-date overview of historical and current view of the pathogenesis and treatment options of atopic dermatitis.