Immunology of atopic eczema: overcoming the Th1/Th2 paradigm

Authors

  • K. Eyerich,

    Corresponding author
    1. ZAUM – Center of Allergy and Environment of the Helmholtz Center and Technische Universität Munich, Munich, Germany
    • Department of Dermatology and Allergy, Technische Universität Munich, Munich, Germany
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  • N. Novak

    1. Department of Dermatology and Allergy, University of Bonn Medical Center, Bonn, Germany
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  • Edited by: Stephan Weidinger

Correspondence

Kilian Eyerich, MD, PhD, Department of Dermatology and Allergy, Biedersteiner Strasse 29, 80802 Munich, Germany.

Tel.: +49-89-41403180

Fax: +49-89-41403453

E-mail: kilian.eyerich@lrz.tum.de

Abstract

Atopic eczema (AE) is a challenge for modern medicine, because it is prevalent, severely affects quality of life of patients and their families, and causes high socioeconomic costs. The pathogenesis of AE is complex. While initial studies suggested a Th2 deviation as primary reason for the disease, numerous studies addressed a genetically predetermined impaired epidermal barrier as leading cause in a subgroup of patients. Recently, immune changes beyond the initial Th2 concept were defined in AE, with a role for specialized dendritic cells as well as newly identified T helper cell subsets such as Th17 and Th22 cells. Furthermore, trigger factors are expanded beyond classical Th2 allergens such as pollen or house dust mites to microbial products as well as self-antigens. This review pieces together our current understanding of immune as well as barrier abnormalities into the pathogenesis mosaic of AE.

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