Abstract
Acute low-dose treatment of murine skin with ultraviolet B (UVB) light impairs induction of contact hypersensitivity (CH) to dinitrofluorobenzene (DNFB) in certain inbred strains of mice (termed UVB-susceptible), but not in others (termed UVB-resistant). These deleterious effects of ultraviolet radiation (UVR) are mediated in part by TNF-α, which is released from UVR-exposed epidermal and dermal cells. To test the hypothesis that polymorphism of TNF-α governs the phenotype of UVB-susceptibility in vivo, various strains of mice received UVB radiation followed by hapten application to induce contact hypersensitivity. Results suggest that the polymorphism at the Tnf-α locus dictates UVB susceptibility in vivo.
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