The exposure of experimental animals to the inflammatory effects of ultraviolet radiation (UVR) is known to cause depressions in their ability to initiate and effectuate various types of cellular immune responses. Contact-type and delayed-type hypersensitivity, plus the ability to generate protective forms of anti-viral and anti-tumor immunity, are all affected by the prior exposure of normal animals to the effects of this physical agent. Presently, the cellular and molecular mechanism(s) responsible for mediating the changes in immune function observed in UVR-exposed animals is not fully understood. Herein we report that one reproducible consequence of exposing normal mice to low doses of UVR is a dramatic change in the pattern of lymphokines secreted by their activated T cells. Lymphocytes isolated from UVR-exposed donors produce/secrete greatly reduced levels of the T cell lymphokines IL-2 and IFN-gamma activation in vitro with protein Ag of the polyclonal T cell stimulant anti-CD3. The secretion of IL-4 by these lymphocyte cultures, however, is consistently elevated in comparison to normal controls. Further studies determined that a similar change in lymphokine production was induced when mice were treated with either bacterial LPS or rIL-1 beta, a cytokine known to be elevated in vivo after UVR or LPS exposure. The ability of IL-1 to facilitate a change in the capacity of T lymphocytes to produce/secrete lymphokines after in vitro activation does not appear to represent a direct effect of this cytokine on lymphocyte or accessory cell targets because addition of IL-1 beta to cultures of Ag-primed lymphocytes obtained from normal donors was incapable of altering the pattern of lymphokine production. Collectively, our present results add further support to the hypothesis that UVR-induced elevations in endogenous IL-1 are, in part, responsible for the immunomodulatory effects of UVR. These findings provide compelling evidence that UVR, plus other agents capable of endogenously stimulating the production of IL-1, may function to alter the expression of different effector mechanisms in vivo. This could be facilitated through selective reductions in lymphokines produced by Th-1-type cells (IL-2 and IFN-gamma) and a simultaneous augmentation in a lymphokine produced by Th-2-type cells (IL-4).