title: Role of Th17 cells in skin inflammation of allergic contact dermatitis.
abstract: Extending the classical concept considering an imbalance exclusively of T helper(h) 1 and Th2 cells on the bottom of many inflammatory diseases, Th17 cells were recently described. Today, there is sufficient experimental evidence to classify psoriasis and allergic contact dermatitis (ACD) amongst other inflammatory skin disorders as IL-17 associated diseases. In several human studies, T-cell-clones could be isolated from eczema biopsies, and high IL-17 levels were observed after challenge with allergen. In the last years, the phenotype of these IL-17 releasing T cells was in the focus of discussion. It has been suggested that Th17 could be identified by expression of retinoic acid receptor-related orphan receptor (ROR)C (humans) or RORγt (mice) and IL-17, accompanied by the absence of IFN-γ and IL-22. In cells from skin biopsies, contact allergens elevate IL-17A, IL-23, and RORC within the subset of Th cells. The indications for a participation of Th17 in the development of ACD are supported by data from IL-17 deficient mice with reduced contact hypersensitivity (CHS) reactions that could be restored after transplantation of wild type CD4(+) T cells. In addition to Th17 cells, subpopulations of CD8(+) T cells and regulatory T cells are further sources of IL-17 that play important roles in ACD as well. Finally, the results from Th17 cell research allow today identification of different skin diseases by a specific profile of signature cytokines from Th cells that can be used as a future diagnostic tool.
authors.affiliation: German Federal Institute for Risk Assessment (BfR), Department of Chemicals Safety, Max-Dohrn-Strasse 8-10, 10589 Berlin, Germany. matthias.peiser@bfr.bund.de
authors.forename: Matthias
authors.initials: M
authors.lastname: Peiser
mesh_terms: D000818:Animals; D017449:Dermatitis, Allergic Contact / Q000276:immunology* / Q000378:metabolism; D006801:Humans; D058504:Th17 Cells / Q000276:immunology* / Q000378:metabolism
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