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Abstract
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.
Declaration of interest
The author has no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Notes
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