Introduction Studies investigating the pathogenesis of atopic eczema (AE) have revealed a central role for pathologic immune responses besides alterations of the vascular, the autonomous nervous, and the skin barrier systems. In contrast to healthy individuals, AE patients appear to develop a T-cell-mediated delayed-type hypersensitivity reaction against certain environmental and, perhaps, self-proteins resulting in an eczema-tous disease. Evidence supporting this concept comes (1) from the successful generation of allergen-specific T-cell clones out of the skin and peripheral blood of AE patients [1-4] and (2) from studies in which environmental antigens applied to tape-stripped skin of sensi-tized AE patients could elicit an eczematous reaction with macroscopic and microscopic similarities to lesio-nal skin of AE patients (atopy patch test) [5]. Our present understanding is that the acute cutaneous allergic inflammation is driven by T helper 2 (Th2) cells that secrete interleukin-4 (IL-4), IL-5, and IL-13. This leads to (1) upregulation of adhesion molecules on endothe-lial cells, (2) chemokine production, and thereby immune-cell recruitment (3) T-cell help for the IgE response, and (4) degranulation of eosinophils [6-9]. Dendritic cells (DC) and/or monocytes/macrophages, as major antigen-presenting cells, are likely to play a key role in determining the outcome of antigen encounter, probably not only during sensitization, but also in established allergic inflammation [10].
CITATION STYLE
Kopp, T., & Stingl, G. (2006). Dendritic Cells in Atopic Eczema. In Handbook of Atopic Eczema (pp. 275–287). Springer-Verlag. https://doi.org/10.1007/3-540-29856-8_27
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