Ultraviolet Light and Suppression of Epidermal Immune Response

There is clear evidence that the keratinocyte does not only represent a mechanical barrier to the outside, but is a fully immunocompetent cell endowed with the capacity to release various immunomodulating cytokines such as interleukin (IL) 1, IL3, IL6, IL8, tumor necrosis factor a, colony stimulating factors (CFS) and several growth factors. The constitutive production of these mediators by keratinocytes both in vivo and in vitro is low, however, can be significantly enhanced by stimuli such as tumor promoters or endotoxin. In addition, ultraviolet (UV)-light has turned out to be one of the most potent inducers of cytokine synthesis and release. Accordingly UV exposure results in an increased production of interleukins, TNF, CSF and growth factors by epidermal cells. The secretion of these cytokines causes local immunologic and inflammatory reactions following UV-irradiation. These factors, however, also may enter the circulation thus being responsible for systemic effects. UV-light also induces keratinocytes to release immunosuppressive factors such as epidermal cell suppressor factor (ECSF), epidermal cell-contra ILI (EC-contra ILI), transforming growth factor β and a recently characterized specific ILI receptor antagonist (IL1ra). Furthermore, upon stimulation with UV-irradiation keratinocytes produce α-melanocyte stimulating hormone (MSHα), a cleavage product of the protein proopiomelanocortin (POMC). MSHα has been shown to block ILI activity and a contact hypersensitivity reaction. The production of such immunoinhibitors may play an essential role during UV-induced immunosuppression.