ABSTRACT
Allergic contact dermatitis is the result of an exaggerated immune response sustained by C D 8 + and CD 4+ type 1 T lymphocytes towards small chemicals penetrating through the skin. Expression of the disease depends upon a coordinated series of events, which include leukocyte extravasation and positioning at the site of hapten penetration, activation of hapten-specific T cells, T cell-mediated apoptosis of keratinocytes and release o f pro inflamma tory cytokines, which modulate the amplification and the persistence of the inflammatory response. Termination of allergic contact dermatitis appears as a necessary event to avoid exces sive tissue damage, and is the consequence of both exhaustion of effector T cells and interven tion of specialized T cell subsets with regulatory functions. Among these, interleukin (IL)-IO producing T regulatory cells 1 and CD 4+CD25+ T lymphocytes have been shown to be ac tively recruited in the skin after hapten challenge and to regulate the magnitude of the allergic reaction.
