Identification of the molecular target for the suppression of contact hypersensitivity by ultraviolet radiation

Détails

ID Serval
serval:BIB_AC62D5079DE3
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Identification of the molecular target for the suppression of contact hypersensitivity by ultraviolet radiation
Périodique
Journal of Experimental Medicine
Auteur(s)
Applegate  L. A., Ley  R. D., Alcalay  J., Kripke  M. L.
ISSN
0022-1007 (Print)
Statut éditorial
Publié
Date de publication
1989
Volume
170
Numéro
4
Pages
1117-1131
Notes
DA - 19891102
LA - eng
PT - Journal Article
PT - Research Support, Non-U.S. Gov't
PT - Research Support, U.S. Gov't, P.H.S
RN - 0 (Pyrimidine Dimers)
RN - 9007-49-2 (DNA)
RN - EC 3.6.1.- (Adenosine Triphosphatases)
RN - EC 4.1.99.3 (Deoxyribodipyrimidine Photo-Lyase)
SB - IM
Résumé
This study was conducted to explore the involvement of DNA damage in the suppression of contact hypersensitivity (CHS) by UV irradiation. The opossum, Monodelphis domestica, was used because cells of these marsupials have an enzyme that is activated by visible light (photoreactivating enzyme) and repairs ultraviolet radiation (UVR)-induced pyrimidine dimers in DNA. A single dose of 1,500 J/m2 of UVB (280-320 nm) radiation, representing 2 minimal erythema doses, was administered to the dorsal skin of opossums. This treatment prevented the opossums from developing a CHS response to dinitrofluorobenze (DNFB) applied either at the site of irradiation or an unirradiated site. In addition, this dose of UVR decreased the number of ATPase+ epidermal Langerhans cells in the dorsal epidermis to approximately 3% of that in unirradiated skin at the time of DNFB application. Treatment of the animals with wavelengths that activate the repair enzyme (320-500 nm, photoreactivating light, PRL) for 120 min immediately after UV irradiation inhibited the UVR-induced suppression of CHS almost completely. Exposure to PRL before UVR did not prevent UVR-induced suppression of CHS. PRL treatment after UV irradiation also prevented the decrease in the number of ATPase+ Langerhans cells. Measurements of lesions in DNA indicated that PRL treatment removed around 85% of the UVR-induced pyrimidine dimers. These data provide direct evidence that DNA, and most likely, the pyrimidine dimer, is the primary molecular target for the UVB-induced suppression of contact hypersensitivity to haptens applied to irradiated or unexposed skin
Mots-clé
Adenosine Triphosphatases/Animals/Cells/Deoxyribodipyrimidine Photo-Lyase/Dermatitis,Contact/Dna/DNA Damage/DNA Repair/enzymology/Epidermis/immunology/Immunosuppression/Langerhans Cells/Light/metabolism/Opossums/physiology/Pyrimidine Dimers/radiation effects/radiotherapy/Skin/Ultraviolet Rays
Pubmed
Web of science
Open Access
Oui
Création de la notice
18/02/2008 18:24
Dernière modification de la notice
20/08/2019 16:16
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