Abstract
Ultraviolet B (UVB) radiation has multiple effects on the immune system, and these effects contribute to the development of UVB-induced skin cancers in mice, and probably man. Depending upon dose and duration of UVB exposure, the resultant immune aberrations may be strictly local (at the irradiated skin site) or systemic. One important local effect of acute, low-dose UVB regimens is impaired induction of contact hypersensitivity (CH). Because a significant proportion of humans who develop CH when hapten is painted on UVB-exposed skin fall to display a primary allergic reaction at that site, we inquired into the effects of UVB radiation on the expression of CH in man. A high proportion of individuals who were first exposed to a sensitizing dose of hapten via UVB-exposed skin displayed CH when challenged on unirradiated (normal) skin 11 d later. However, only 50% of these subjects developed CH when challenged simultaneously on skin that had been exposed to UVB radiation 11 d previously. Because the density of epidermal antigen-presenting cells was comparable in both responders and non-responders, we interpret these findings to mean that UVB radiation can create a sustained immunosuppressive microenvironment that inhibits the expression of CH. In separate experiments, when normal volunteers were sensitized with hapten via unirradiated (normal) skin, expression of CH at UVB-exposed challenge sites 11 d later was found to be enhanced, at least in some individuals, compared to expression of CH at unirradiated challenge sites. Thus, the local effects of UVB radiation on expression of CH in man may be enhancing or inhibitory, depending upon whether initial sensitization occurred through normal or through UVB-exposed skin.
Published Version
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