Abstract
Atopic dermatitis is a chronic inflammatory skin disease frequently seen in individuals with a genetic predisposition to increased IgE synthesis and IgE-mediated allergic reactions. However, the role of IgE in the pathomechanisms of atopic dermatitis remains unclear. The high affinity IgE receptor (FcεRI) is expressed on two distinct groups of cells: effector cells of anaphylaxis, i.e., mast cells, basophils; and antigen presenting cells such as Langerhans cells and monocytes/macrophages. FcεRI enables them to efficiently present antigen in IgE-mediated delayed-type hypersensitivity. In addition, FcεRI mediates various, unexpected activating signals in these cells which contribute to inflammatory reactions and chronicity of atopic dermatitis. Modulation of FcεRI-mediated signals may be a promising strategy for treating atopic disease.
