Abstract

Ultraviolet-B (UVB), in addition to direct effects on DNA, induces immunological changes in the skin that predispose to the development of skin cancer. Whether ultraviolet-A (UVA) induces similar changes is unknown. This effect can be investigated in humans in vivo using epicutaneous antigens as a model of tumour antigens. Volunteers (n = 46) were randomly assigned to received no sensitization, sensitization with the allergen diphenylcyclopropenone (DPCP) on non-UV-exposed normal skin, or sensitization with DPCP on skin exposed to three minimal erythema doses (MED) of either UVA or UVB radiation 3 days before sensitization. Three weeks after sensitization all volunteers were challenged with five different concentrations of DPCP. The challenge reactions were scored clinically and the increase in skin thickness was measured using a micrometer. Sensitization on UVB-exposed skin reduced the immunization rate compared with sensitization on non-irradiated skin (P < 0.03) as previously described. In contrast, sensitization on skin exposed to three MED UVA radiation did not result in a decreased immunization rate compared with non-irradiated skin. These results indicate that in humans erythemagenic doses of UVA radiation do not reduce the immunization rates to epicutaneous allergens. Thus UVB and UVA irradiation have contrasting effects on cell-mediated immunity in humans. These findings may at least in part explain the less carcinogenic effect of UVA irradiation.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.