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UV radiation was found to enhance the release by keratinocytes of epidermal cell thymocyte-activating factor (ETAF), a hormone-like molecule that is physiochemically identical to interleukin 1 (IL-1). This conclusion was supported by the following observations: (i) the keratinocyte cell line PAM 212 retained ETAF/IL-1-producing potential after exposure to UV radiation despite significant loss in cell viability; (ii) epidermal cells from normal and UV radiation-exposed mice were found to produce equivalent amounts of ETAF/IL-1 on a per cell basis with the density of epidermal cells in UV radiation-exposed skin being at least 5-fold above normal values; (iii) under the conditions used, ETAF/IL-1 could be detected in the serum of UV radiation-exposed, but not normal, animals; and (iv) many of the biologic consequences known to be mediated by elevations in ETAF/IL-1--i.e., neutrophilia, elevated levels of complement component 3, serum amyloid P, and plasma fibrinogen--were all observed in animals following a single UV radiation exposure. Animals subjected to chronic UV radiation showed an initial elevation in their levels of acute-phase reactants that returned to normal concentrations within 7 days. This correlates with observations made by others of a "desensitization" to ETAF/IL-1-mediated effects after chronic administration of known exogenous stimulators of inflammatory responses. Further, the UV radiation-induced desensitization took place in spite of demonstrable serum levels of ETAF/IL-1. These results suggest that the mechanism(s) responsible for desensitization is not an inhibition of ETAF/IL-1 synthesis but rather may result from inability of the target cells to perceive this endogenous mediator or to unavailability of serum-associated ETAF/IL-1 for the appropriate targets.

Effect of ultraviolet radiation on production of epidermal cell thymocyte-activating factor/interleukin 1 in vivo and in vitro.