Die Rolle dendritischer Zellen bei der atopischen Dermatitis

Abstract

Atopic dermatitis (AD) presents as a chronic relapsing skin disease with a characteristic phenotype and typically distributed skin lesions, which make the diagnosis of AD very simple and clear-cut. In contrast, the underlying pathophysiological and genetic mechanisms leading to the manifestation of AD are not obvious. Challenged by this puzzle, scientific approaches of the last years have made considerable progress in gaining insights into the complexity of the mechanisms which cause AD. AD is a biphasic inflammatory skin disease characterized by an initial phase predominated by Th2 cytokines which switches into a second and more chronic Thl-dominated eczematous phase. Two different, the high affinity receptor for IgE(FceRI)-bearing dendritic cell subtypes have been identified in the skin of AD patients: FceRI + Langerhans cells (LC) and FceRI + inflammatory dendritic epidermal cells (IDEC). These dendritic cell subtypes are supposed to contribute distinctly to the biphasic nature and the outcome of T cell responses in AD. In contrast, plasmacytoid dendritic cells which have been shown to bear the high affinity receptor for IgE very recently and which play an important role in the defense against viral infections, are nearly absent from the skin lesions of AD patients. In the light of recent developments, a picture emerges that different IgE receptor-bearing DC subtypes in the blood and the skin of AD patients play a pivotal role in the complex pathophysiological network of AD.