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Abnormal skin barrier in the etiopathogenesis of atopic dermatitis

Elias, P.M.; Schmuth, M. Current Opinion in Allergy and Clinical Immunology 9(5):437-446, 01/10/2009

Purpose of review Many recent studies have revealed the key roles played by Th1/Th2 cell dysregulation, IgE production, mast cell hyperactivity, and dendritic cell signaling in the pathogenesis of atopic dermatitis. Accordingly, current therapy has been largely directed towards ameliorating Th2-mediated inflammation and/or pruritus.

We will review here emerging evidence that the inflammation in atopic dermatitis results from inherited and acquired insults to the barrier and the therapeutic implications of this new paradigm. Recent findings Recent molecular genetic studies have shown a strong association between mutations in FILAGGRIN and atopic dermatitis, particularly in Northern Europeans. But additional acquired stressors to the barrier are required to initiate inflammation. Sustained hapten access through a defective barrier stimulates a Th1 -> Th2 shift in immunophenotype, which in turn further aggravates the barrier, Secondary Staphylococcus aureus colonization not only amplifies inflammation but also further stresses the barrier in atopic dermatitis. Summary These results suggest a new ‘outside-to-inside, back to outside’ paradigm for the pathogenesis of atopic dermatitis. This new concept is providing impetus for the development of new categories of ‘barrier repair’ therapy.

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Acerca de PIEL-L

Mesa de redacción de Piel Latinoamericana. Donde recibimos casos, aportes e información de interés para la comunidad latinoamericana dermatólogica

2 comentarios

  1. Estimados editores sería de gran utilidad el disponer de este artículo.

    Se agradece su constante preocupación en la promoción de la educación médica

    Guillermo Pino

  2. Ma Eugenia Moreno, Puebla/Mexico

    Concuerdo con el Dr Pino que conviene tener el articulo completo.

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