Molecular Basis of Photoimmunologic Effects

Abstract

Ultraviolet (UV) light can suppress the immune system both in a local and systemic fashion. Numerous experimental models exist to study the immunosuppressive effects of UV light (Kripke, 1990). The most commonly used is the suppression of the induction of contact hypersensitivity in mice. Sensitization with haptens through UV-exposed skin does not result in contact hypersensitivity but induces hapten specific immune tolerance (Toews et al, 1980). Since this immune tolerance can be transferred by injecting T cells from tolerized mice into naive animals, T suppressor cells are supposed to be involved in this process (Elmets et al, 1983). Numerous studies of the last two decades have shown that immunosuppression by UV light is a complex process in which several different pathways appear to be involved. UV light can inhibit the function of antigen presenting cells and deplete Langerhans cells from the epidermis (Aberer et al, 1981), presumably by inducing apoptosis. UV light can induce the release of inflammatory cytokines including interleukin-1, interleukin-6, tumor necrosis factor and others which contribute to UV-mediated inflammation (Kupper et al, 1987; Kirnbauer et al, 1991; Köck et al, 1990). These mediators, however, enter also the circulation and thereby cause systemic sunburn reaction which is associated with fever, chills, leukocytosis and induction of an acute phase protein response (Urbanski et al, 1990). In addition, UV light was found to induce the release of mediators with immunosuppressive properties (Schwarz et al, 1986).