Modulation of IL-10, IL-12, and IFN-γ in the epidermis of hairless mice by UVA (320-400 nm) and UVB (280-320 nm) radiation

We have observed recently that the suppression of contact hypersensitivity (CHS) induced in mice by UVB irradiation may be prevented by suberythemal exposure to UVA radiation. Because the UVB-immunosuppressed state is associated with an upregulation of the Th2-associated cytokines IL-10 and IL-4, and a deficiency in Th1-associated IL-2, IL-12, and IFN-gamma, and because UVA photoimmunoprotection appeared to be IFN-gamma- dependent, we tested the hypothesis that UVA immunoprotection results from an ability to prevent the UVB-induced cytokine disarray, This study describes changes in epidermal IL-10, IL-12 and IFN-gamma for 5 d following irradiation of hairless mice with the CHS-modulating doses of UVB, UVA, or UVA + UVB, using immunohistochemical detection in paraffin embedded skin sections, followed by image analysis quantitation, We found that UVB, but not UVA exposure, caused an increase in epidermal IL-10 expression, peaking at 3 d, UVA irradiation, but not UVB, resulted in increased epidermal IL-12 expression, peaking at 3 d, and increased epidermal IFN-gamma expression peaking earlier at 1 d, Irradiation with UVA + UVB abrogated the UVB-enhanced expression of IL-10, and caused small but significant increases in IL-12 and IFN-gamma at 3 d and 1 d, respectively. These findings suggest that UVA photoimmunoprotection is mediated via prevention of IL-10 release, and thus the maintenance of the Th1/Th2 balance, probably by upregulation of IL-12 and IFN-gamma, which are known to antagonize IL-10 in numerous models. The time course suggests that IFN-gamma responds initially to WA radiation, and may stimulate the increased expression of IL-12.