title: Therapeutic strategies in extrinsic atopic dermatitis: focus on inhibition of IL-4 as a new pharmacological approach.
abstract: BACKGROUND
  Recent data about atopic dermatitis (AD) pathogenesis postulate that T cells and their related cytokines and chemokines are primarily responsible for the inflammatory responses.
  
  
  METHODS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Arcispedale Santa Maria Nuova-IRCCS, Dermatology Unit , viale Risorgimento 68, 42123 Reggio Emilia , Italy.
authors.forename: Vito
authors.initials: V
authors.lastname: Di Lernia
mesh_terms: D000818:Animals; D003876:Dermatitis, Atopic / Q000188:drug therapy* / Q000235:genetics / Q000276:immunology; D000091344:Filaggrin Proteins; D006801:Humans; D015847:Interleukin-4 / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000276:immunology
chemical_list: C000717249:FLG protein, human; D000091344:Filaggrin Proteins; D015847:Interleukin-4
keywords: IL-13; IL-4; atopic dermatitis; cytokines; inhibition; treatment