¹Faculty of Veterinary Science, University of Sydney, Sydney, New South Wales, Australia

Correspondence: Dr Vivienne Reeve, Faculty of Veterinary Science, University of Sydney, McMaster Building B14, Sydney, New South Wales 2006, Australia. E-mail: vreeve@usyd.edu.au

Received 20 October 2008; Revised 4 February 2009; Accepted 24 February 2009; Published online 28 May 2009.

Abstract

Previous studies have found that signaling by the estrogen receptor- (Er-) attenuated solar-simulated UV radiation (SSUV)-induced immunosuppression. This study seeks evidence for a common mechanism for this immunoprotection for both Er- signaling and irradiation with the UVA waveband. In Skh:hr-1 hairless mice, the immunoprotection afforded by UVA exposure against subsequent UVB or cis-urocanic acid suppression of contact hypersensitivity (CHS) was abrogated by treatment with the antiestrogen, ICI 182,780. Furthermore, in normal C57BL mice, UVA enrichment of UVA/UVB sources provided protection against UVB-suppressed CHS and upregulated epidermal IL-10 expression, but this protection was inhibited in Er--/- mice. These observations indicated that the immunoprotective response to UVA was dependent on Er- signaling. As earlier studies have established that UVA photoimmune protection depends on the induction of the stress enzyme, heme oxygenase (HO)-1, its activity was examined relative to Er-. Immunoprotection against SSUV by 17--estradiol was prevented by inhibiting HO enzyme activity; immunoprotection against cis-urocanic acid by carbon monoxide (HO product) was prevented by ICI 182,780. In addition, the HO-1 gene was unresponsive to UVA induction in Er--/- mice. Therefore, HO-1 inducibility and Er- signaling are interdependent requisite responses to the UVA waveband for its immunoprotective action against UVB exposure.