Therapeutic strategies in extrinsic atopic dermatitis: focus on inhibition of IL-4 as a new pharmacological approach

Introduction: Recent data about atopic dermatitis (AD) pathogenesis postulate that T cells and their related cytokines and chemokines are primarily responsible for the inflammatory responses.

Areas covered: AD, the primary complex disease associated with filaggrin deficiency, is characterized by cutaneous inflammation driven by type 2 helper T (TH2) cells. TH2-related molecules, such as IL-4, IL-13, dominate the immune infiltrate. Experimental evidences suggest that these cytokines may be considered attractive therapeutic targets in AD, particularly in extrinsic AD with IgE overproduction. Recently, a fully human monoclonal antibody directed against the IL-4 receptor α subunit blocking IL-4 and IL-13 signaling has been evaluated in Phase I and Phase II clinical trials in patients with moderate-to-severe AD with significant improvement in disease severity. Phase III trials are ongoing.

Expert opinion: Treatment of AD represents a therapeutic challenge. TH2 cytokine-targeted therapies represent promising treatment options that could improve the therapeutic armamentarium for AD. These therapies are likely to become future therapeutic options in AD, particularly in the extrinsic AD.