1. Department of Microbiology and Infectious Diseases, School of Medicine, Flinders University, Adelaide, Australia
2. ^*Department of Medicine (Dermatology), University of Sydney, Australia

Correspondence: Dr Prue Hart, Department of Microbiology & Infectious Diseases, School of Medicine, Flinders University, GPO Box 2100, Adelaide, Australia 5001. Email: prue.hart@flinders.edu.au

Received 12 July 1999; Revised 13 December 1999; Accepted 13 December 1999.

Abstract

Ultraviolet B radiation is immunosuppressive by multiple mechanisms. In interleukin-4–/– mice, ultraviolet B radiation was not able to suppress delayed-type hypersensitivity or contact hypersensitivity responses when the sensitizing antigen was applied to nonirradiated sites. In contrast, ultraviolet B significantly suppressed contact hypersensitivity responses to haptens applied to irradiated sites in interleukin-4–/– mice. In mast cell depleted Wf/Wf mice, ultraviolet B radiation also significantly suppressed contact hypersensitivity responses to sensitizing antigens applied to irradiated but not to unirradiated sites. In both interleukin-4–/– mice and Wf/Wf mice, the mast cell product, histamine, was immunosuppressive implicating mast cells as the dysfunctional cell in interleukin-4–/– mice. The prevalence of dermal mast cells was similar in wild-type and interleukin-4–/– mice. Dermal mast cells of interleukin-4–/– mice, however, express very low levels of c-kit and did not significantly degranulate in response to ultraviolet B. Ultraviolet radiation induced significant and similar levels of serum interleukin-10 in wild-type and interleukin-4–/– mice. We conclude that interleukin-4 indirectly affects ultraviolet B suppression of contact hypersensitivity and delayed-type hypersensitivity responses to sensitizing antigens applied at sites other than those irradiated by providing a critical differentiative signal for dermal mast cells. This study further emphasizes the central role of mast cells in the initial processes by which ultraviolet B radiation is immunomodulatory for immune responses to sensitizing antigens applied to nonirradiated sites.