title: Involvement of prostaglandins in the immune alterations caused by the exposure of mice to ultraviolet radiation.
abstract: Our study was designed to analyze the possible involvement of prostaglandins in the mechanisms responsible for the depressions in contact hypersensitivity (CH) responsiveness observed in UVR-exposed animals. Low-dose UVR-exposed animals were found to exhibit a depressed capacity to elicit CH responses after hapten application to irradiated (devoid of Langerhans cells) or UVR-protected (normal Langerhans cells) dorsal skin surfaces. Normal responsiveness was observed in low-dose UVR-exposed animals sensitized through unirradiated ventral skin surfaces. Indomethacin treatment of low-dose UVR-exposed animals (to inhibit prostaglandin synthesis in vivo) caused a retention in the capacity to respond normally to CH induction to haptens applied to the nonirradiated, but not to irradiated, dorsal skin surfaces. High-dose UVR-exposed animals, which normally exhibit a depression in responsiveness to hapten sensitization, retained a normal capacity to elicit CH responses if treated with the drug indomethacin. These findings implicate prostaglandins in the pathogenesis of the immunologic hyporesponsiveness, observed in low- and high-dose UVR-exposed animals. Our studies also determined that under all experimental conditions where animals were contact sensitized through nonirradiated skin sites, CH-effector cells could be found in the draining lymph nodes. No CH-effector cells were observed in the lymph nodes of mice that were contact sensitized directly through irradiated skin sites. It was also found that the spleens of both UVR-exposed and normal animals contained adoptively transferrable suppressor cells subsequent to hapten application. This demonstration of CH-effector and CH-suppressor cells in both normal and UVR-exposed animals did not directly relate to the potential of the donor animals to elicit a CH response.
authors.forename: H T
authors.initials: HT
authors.lastname: Chung
authors.forename: D K
authors.initials: DK
authors.lastname: Burnham
authors.forename: B
authors.initials: B
authors.lastname: Robertson
authors.forename: L K
authors.initials: LK
authors.lastname: Roberts
authors.forename: R A
authors.initials: RA
authors.lastname: Daynes
mesh_terms: D000818:Animals; D003877:Dermatitis, Contact; D005260:Female; D000949:Histocompatibility Antigens Class II / Q000032:analysis; D007116:Immunization, Passive; D007165:Immunosuppression Therapy; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D011453:Prostaglandins / Q000276:immunology*; D012867:Skin / Q000276:immunology* / Q000528:radiation effects; D014466:Ultraviolet Rays
chemical_list: D000949:Histocompatibility Antigens Class II; D011453:Prostaglandins; D007213:Indomethacin