title: Ultraviolet B-induced suppression of immune responses in interleukin-4-/- mice: relationship to dermal mast cells.
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.
authors.affiliation: Department of Microbiology and Infectious Diseases, School of Medicine, Flinders University, Adelaide, Australia. prue.hart@flinders.edu.au
authors.forename: P H
authors.initials: PH
authors.lastname: Hart
authors.forename: M A
authors.initials: MA
authors.lastname: Grimbaldeston
authors.forename: A
authors.initials: A
authors.lastname: Jaksic
authors.forename: J E
authors.initials: JE
authors.lastname: Tan
authors.forename: G J
authors.initials: GJ
authors.lastname: Swift
authors.forename: E K
authors.initials: EK
authors.lastname: Hosszu
authors.forename: G M
authors.initials: GM
authors.lastname: Halliday
authors.forename: J J
authors.initials: JJ
authors.lastname: Finlay-Jones
mesh_terms: D000818:Animals; D000917:Antibody Formation / Q000528:radiation effects*; D002452:Cell Count; D015550:Cell Degranulation; D003877:Dermatitis, Contact / Q000209:etiology; D006968:Hypersensitivity, Delayed / Q000473:pathology; D016753:Interleukin-10 / Q000097:blood; D015847:Interleukin-4 / Q000032:analysis*; D008407:Mast Cells / Q000166:cytology / Q000276:immunology / Q000528:radiation effects; D051379:Mice; D008810:Mice, Inbred C57BL; D010853:Picryl Chloride / Q000276:immunology; D012867:Skin / Q000166:cytology / Q000528:radiation effects; D013154:Spleen / Q000166:cytology; D014466:Ultraviolet Rays
chemical_list: D016753:Interleukin-10; D015847:Interleukin-4; D010853:Picryl Chloride