Abstract
Human antigen-presenting cells (APCs) bind monomeric immunoglobulin E (IgE) via the high-affinity IgE receptor, Fc epsilon RI. Surface expression of this trimeric structure is strongly associated with the atopic status of the donors, and maximal levels are observed on Langerhans cells (LC) and inflammatory dendritic epidermal cells (IDEC) in atopic dermatitis (AD). Although intracellular expression of the Fc epsilon RI alpha-chain is induced by interleukin-4 (IL-4), the upregulation of surface levels on dendritic cells (DC) from atopics is due to enhanced expression of the Fc epsilon RI gamma-chain and stabilization by binding of its ligand IgE. A characteristic function of Fc epsilon RI-bearing APCs is the specific uptake and processing of IgE-bound allergens, which is followed by T-cell stimulation. In AD, DC-mediated presentation of aeroallergens penetrating the epidermis is thought to induce an IgE-mediated, delayed-type hypersensitivity reaction. In addition, different Fc epsilon RI-bearing APC subsets in AD skin might regulate inflammatory processes through the production of Th1/Th2-polarizing signals, proinflammatory cytokines, chemokines, and factors that are involved in the induction of tolerance.
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