Interactions between the UVA and UVB wavebands relevant for immune function and carcinogenesis

Abstract

Exposure of the skin of mice and men to increasing doses of UV radiation causes erythema, chronic hyperplasia, mutation, accelerated photo-ageing and photocarcinogenesis. Moderate exposure also suppresses T cell-mediated immune function, a defect which is a prerequisite for the promotion or outgrowth phase of the UV-initiated tumour. This immunosuppressed state is accompanied by dysregulated cutaneous cytokine patterns, particularly a relative deficit of Th1-type cytokines like interleukin (IL)-12 and interferon-γ (IFN-γ). The cutaneous photoreceptor for the immunosuppression may be either, or both, epidermal DNA or urocanic acid (UCA). Naturally occurring trans-UCA photo-isomerises in the stratum corneum and epidermis to cis-UCA, which has local and systemic immunosuppressive properties. The action spectrum for the photo-immunosuppression is maximal in the UVB (280–320 nm) waveband. However, longer wavelength UVA (320–400 nm), which interacts with skin predominantly via oxidative reactions, is not immunosuppressive at environmental exposure doses and, unexpectedly, as we have demonstrated in several strains of mice and opossums, can provide protection from UVB immunosuppression.¹