UVA-induced immune suppression through an oxidative pathway.

Although ultraviolet B (UVB) irradiation induces local immune or systemic immune suppression, depending on the dose, the immune suppression by ultraviolet A (UVA) has not been fully investigated. In this study, we investigated the effect of UVA on the immune response in vitro and in vivo. The effect of UVA on the antigen-presenting function of epidermal cells was measured in terms of antigen-specific T cell proliferation. A murine epidermal cell suspension was exposed to UVA in vitro, pulsed with trinitrobenzenesulfonic acid, and cultured with T cells prepared from syngeneic mice previously sensitized with trinitrochlorobenzene. UVA (5-20 J per cm2) suppressed the antigen-presenting function of epidermal cells in a dose-dependent manner, accompanied with suppression of the expression of costimulatory molecules on Langerhans cells. In order to investigate the effect of an antioxidant on the immune suppression, an epidermal cell suspension was irradiated with UVA in the presence or absence of glutathione. The suppressions of antigen-presenting function and ICAM-1 expression were significantly prevented by glutathione in a dose-dependent manner. Further, the effect of UVA on the immune response at the induction phase of contact hypersensitivity was evaluated in terms of lymph node cell proliferation ex vivo. UVA irradiation suppressed the endogenous proliferation of lymph node cells in trinitrochlorobenzene-painted mice, and this suppression was significantly reversed by the application of glutathione to the skin during irradiation. These results suggest that UVA-induced immune suppression may be mediated by reactive oxygen species, at least in part.