Inhibition of IL-4 may be useful in atopic dermatitis.

What is it about?

The identification of driver cytokines is a priority in the development of new therapeutic concepts against AD. Th2 immunity seems to be the end stream of a heterogeneous group of conditions with the clinical phenotype of AD. In acute lesions of AD, the Th2 cells produce IL-4, IL-13, and IL-31, which may potentiate barrier dysfunction and contribute to pruritus. In chronic lesions, a distinct T-cell infiltrate with Th1, Th17 and Th22 is present. Preliminary data suggest that blockade of IL-4 and IL-13 signaling may be an attractive therapeutic target for AD.

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Why is it important?

Adult patients with atopic dermatitis may be included in dermatologic areas with a high unmet medical need. Systemic agents for the treatment of moderate-to-severe atopic dermatitis have not been developed in the last two decades. Treatment options for refractory AD consist of phototherapy and broad spectrum immunosuppressant, sometimes in an off-label basis. Development in defining immunogenetics and pathomechanisms of atopic dermatitis takes with it the demand to understand better the clinical spectrum of disease. The biologic revolution in therapy of inflammatory diseases is going to involve atopic dermatitis, bringing with it an urgent need for rational drug design based on known biological targets.

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