title: Parallel recovery of epidermal antigen-presenting cell activity and contact hypersensitivity responses in mice exposed to ultraviolet irradiation: the role of a prostaglandin-dependent mechanism.
abstract: Contact hypersensitivity (CH) responsiveness to 2-4-dinitro-1-fluorobenzene (DNFB) is depressed in mice that are sensitized through skin sites exposed to ultraviolet radiation (UVR). This is partially due to a reduction in antigen-presenting cell (APC) activity within UVR-exposed skin, a condition marked by a decrease in the density of ATPase/Ia-positive epidermal cells. The purpose of this study was to correlate the histological and functional recovery of APC activity in the skin of C3H mice exposed to low-dose (4 X 450 J/m2) or high-dose (1 X 15 kJ/m2) UVR with the normalization of CH responsiveness. Skin biopsy specimens taken at various intervals after UVR exposure revealed a rapid recovery in the density of ATPase/Ia positive cells: about 70% of normal by 3 days, and normal after 5 days. Functional analyses showed that lymph node cells obtained from donors that were sensitized with DNFB 3 days after UVR treatment transferred normal ear-swelling responsiveness to non-primed recipients, thus indicating that APC activity in UVR-exposed skin paralleled the recovery of ATPase/Ia-positive epidermal cells. This suggested that an alternative mechanism causes the persistent depression of CH in mice exposed to UVR. Mice pretreated with indomethacin prior to UVR exposure demonstrated a capacity to elicit CH responses to DNFB, which paralleled the histological and functional recovery of APC in the skin (i.e., normal CH responses were elicited 3 days after exposure to UVR). We conclude from this study that APC activity in the skin recovers rapidly after exposure to UVR, and that a PG-dependent mechanism is responsible for many of the persistent and systemic effects that cause a depression in the CH responsiveness of mice treated with UVR.
authors.affiliation: Department of Internal Medicine (Division of Dermatology), University of Utah School of Medicine, Salt Lake City 84132.
authors.forename: B D
authors.initials: BD
authors.lastname: Jun
authors.forename: L K
authors.initials: LK
authors.lastname: Roberts
authors.forename: B H
authors.initials: BH
authors.lastname: Cho
authors.forename: B
authors.initials: B
authors.lastname: Robertson
authors.forename: R A
authors.initials: RA
authors.lastname: Daynes
mesh_terms: D000251:Adenosine Triphosphatases / Q000032:analysis; D000818:Animals; D000938:Antigen-Presenting Cells / Q000276:immunology / Q000528:radiation effects*; D003877:Dermatitis, Contact / Q000276:immunology*; D004307:Dose-Response Relationship, Radiation; D005260:Female; D000949:Histocompatibility Antigens Class II / Q000032:analysis; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D011453:Prostaglandins / Q000502:physiology*; D012867:Skin / Q000276:immunology*; D014466:Ultraviolet Rays
chemical_list: D000949:Histocompatibility Antigens Class II; D011453:Prostaglandins; D000251:Adenosine Triphosphatases; D007213:Indomethacin