Ultraviolet B-induced suppression of immune responses in interleukin-4-/-mice: Relationship to dermal mast cells

Ultraviolet B radiation is immunosuppressive by multiple mechanisms. In int erleukin-4-/- mice, ultraviolet B radiation was not able to suppress delaye d-type hypersensitivity or contact hypersensitivity responses when the sens itizing antigen was applied to nonirradiated sites. In contrast, ultraviole t 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 bu t not to unirradiated sites. In both interleukin-4-/- mice and Wf/Wf mice, the mast cell product, histamine, was immunosuppressive implicating mast ce lls as the dysfunctional cell in interleukin-4-/- mice. The prevalence of d ermal 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. Ul traviolet radiation induced significant and similar levels of serum interle ukin-10 in wild-type and interleukin-4-/- mice. We conclude that interleuki n-4 indirectly affects ultraviolet B suppression of contact hypersensitivit y and delayed-type hypersensitivity responses to sensitizing antigens appli ed at sites other than those irradiated by providing a critical differentia tive signal for dermal mast cells. This study further emphasizes the centra l role of mast cells in the initial processes by which ultraviolet B radiat ion is immunomodulatory for immune responses to sensitizing antigens applie d to nonirradiated sites.