FcεRI Mediates IgE-Binding to Human Epidermal Langerhans Cells
In 1986, it was first recognized that epidermal Langerhans cells (LC) in lesional and non-lesional skin of atopic dermatitis (AD) patients have IgE-binding capacity (1,2). Furthermore, it was shown that, after acid-stripping of cell-bound IgE, the anti-IgE reactivity of LC can be restored by incubation of tissue substrates with native, but not with heated autologous IgE-rich serum (1). In view of the heat lability of the Fc∊ fragment, this observation led to the concept that IgE binds to LC via its Fc∊ fragment (1). Since exposure of LC-enriched epidermal cells from non-atopies to IL-4 and/or IFN-γ leads to the surface expression of anti-FceRII/CD23-reactive moieties on LC (3), it was originally thought that LC in AD skin bind IgE via FcεRII/CD23 induced by cytokines present in the AD skin microenvironment. However, IgE+ LC were subsequently also detected in other diseases, provided that the serum IgE level exceeded 100kU/L (4). It was therefore reasonable to assume that the presence of IgE-binding sites on human epidermal LC is not a consequence of the respective disease process, but rather represents a constitutive property of these cells.
KeywordsMast Cell Atopic Dermatitis Atopic Dermatitis Skin Haemopoietic Growth Factor Vienna Medical School
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