Ultraviolet A Radiation (320–400 nm) Protects Hairless Mice from Immunosuppression Induced by Ultraviolet B Radiation (280–320 nm) or <i>Cis-</i>Urocanic Acid

Abstract

T cell-mediated immune function, here measured as the contact hypersensitivity reaction, is readily suppressed by moderate exposure of mice to ultraviolet B (UVB) or solar-simulated radiation (SSUV), or by topical application of cis-urocanic acid. The effect of ultraviolet A (UVA) radiation on immune function has been unclear. Here we have demonstrated that when UVA radiation from a fluorescent tube source was rigorously filtered to remove contaminating UVB radiation, it was immunologically innocuous at physiologically relevant doses. Furthermore, we have found that mice exposed to UVA radiation, either immediately after, or up to 24 h before, immunosuppressive treatment with either UVB radiation, SSUV or cis-urocanic acid, became refractory to the immunosuppression and retained more normal contact hypersensitivity. A greater UVA exposure reversed the immunosuppression more effectively. The results suggest that there are immunologically significant interactions between UV wavebands, and that UVA exposure may induce a relatively long-lived immunoprotective photoproduct, as yet unidentified, that can inhibit the activity of epidermal cis-urocanic acid and thus provide protection from photoimmunosuppression.

Heme oxygenase induction mediates the photoimmunoprotective activity of UVA radiation in the mouse

“…We have speculated that the mechanism of UVA photoimmunoprotection involves a UVA photoproduct that is relatively stable and persists for at least 24 h in the cutaneous environment, perhaps localized in the dermis where it would be preferentially produced by UVA rather than UVB radiation (10). This study has tested the hypothesis that induced HO-1 acts in this role and has shown that, whereas there is measurable HO enzyme activity present constitutively in hairless mouse skin, cutaneous HO activity is also UVA inducible and remains elevated for a period of at least 3 d after UVA irradiation.…”

“…However, exposure to such UVA radiation induced a state of resistance in the mice to the immunosuppressive effects of either UVB radiation or cis-UCA (10), both of which could be applied before, immediately after, or up to 24 h after the UVA radiation. We postulated that UVA exposure may induce a relatively long-lived, but as-yet-unidentified, immunoprotective photoproduct that can inhibit the activity of cis-UCA and thus provide protection from UVB-induced photoimmunosuppression.…”

UVA and UVB wavebands modulate expression ofFasLin mouse skin epidermis

“…We have found in mice that UVA irradiation protects from UVB-induced immunosuppression. 1 We observed different cytokine modulation in mouse epidermis by the UVA and UVB wavebands: UVA acts as an inducer of Th1-derived cytokines like IL-12 and IFN-γ, while UVB is responsible for induction of Th2-derived cytokines like IL-10, a major cause of immunosuppression. 2 However, the underlying mechanism(s) by which UVA achieved immunoprotection against UVB have remained undefined.…”

“…1 Mouse skins were fixed, processed and paraffin embedded immediately and at 24 hourly intervals for 5 days post-irradiation. FasL antibody was used to detect FasL expression in mouse skin by immunohistochemistry.…”

UVA-induced protection of skin through the induction of heme oxygenase-1

“…They indicated that the mechanism of UVA immunoprotection involves the induction of cutaneous HO-1 (37,38). Moreover, they reported that UVA irradiation upregulated HO-1 in the dermis and epidermis of hairless mouse skin, and UVA-induced HO enzyme activity is protective against UVB-induced immunosuppression (10,39).…”