[The significance of epidermal cytokines in UV-induced immune suppression].

Using experimental animals it has been well demonstrated that UVB exposure leads to local and systemic immunosuppression. With regard to the local form, epidermal Langerhans cells appear to be the main target as they lose their antigen-presenting capacity after UVB exposure. During the last few years the pathomechanisms involved in systemic immunosuppression have been studied intensively, as their clarification may reveal new photoimmunological aspects and therapeutic possibilities. It could be demonstrated that keratinocytes exhibit the capacity to release immunosuppressive factors in addition to immunostimulating cytokines, such as interleukin I. UV-irradiated cultured keratinocytes release a low-molecular-weight factor which, when injected intravenously, blocks the induction of contact hypersensitivity. Moreover, under identical conditions keratinocytes produce a second, possibly related cytokine, which suppresses the biological activity of interleukin I, an important mediator of immunological and inflammatory reactions. These observations demonstrate that keratinocytes may participate in the regulation of the epidermal immune response through the release of both immunostimulating and immunosuppressive cytokines. The characterisation of these mediators may yield new insight into the mechanisms of allergy and photocarcinogenesis. Moreover, the therapeutic application of these "physiological immunosuppressors" might reveal new aspects concerning selective immunosuppression.