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Department of Immunology, University of Texas, M. D. Anderson Cancer Center, and Graduate School of Biomedical Sciences, Houston, TX 77030
UV-induced immune suppression is a risk factor for sunlight-induced
skin cancer. Exposure to UV radiation has been shown to suppress the
rejection of highly antigenic UV-induced skin cancers, suppresses
delayed and contact hypersensitivity, and depress the ability of
dendritic cells to present Ag to T cells. One consequence of UV
exposure is altered activation of T cell subsets. APCs from
UV-irradiated mice fail to present Ag to Th1 T cells; however, Ag
presentation to Th2 T cells is normal. While this has been known for
some time, the mechanism behind the preferential suppression of Th1
cell activation has yet to be explained. We tested the hypothesis that
this selective impairment of APC function results from altered cytokine
production. We found that dendritic cells/macrophages (DC/M
) from
UV-irradiated mice failed to secrete biologically active IL-12
following in vitro stimulation with LPS. Instead, DC/M isolated from
the lymphoid organs of UV-irradiated mice secreted IL-12p40 homodimer,
a natural antagonist of biologically active IL-12. Furthermore, when
culture supernatants from UV-derived DC/M were added to
IL-12-activated T cells, IFN-
secretion was totally suppressed,
indicating that the IL-12p40 homodimer found in the supernatant fluid
was biologically active. We suggest that by suppressing DC/M
IL-12p70 secretion while promoting IL-12p40 homodimer secretion, UV
exposure preferentially suppress the activation of Th1 cells, thereby
suppressing Th-1 cell-driven inflammatory immune
reactions.
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