Epidermal Urocanic Acid and Suppression of Contact Hypersensitivity by Ultraviolet Radiation in Monodelphis domestica

1996 ◽  
Vol 109 (3) ◽  
pp. 266-271 ◽  
Author(s):  
V.E. Reeve ◽  
R.D. Ley ◽  
W.G. Reilly ◽  
M. Bosnic
Keyword(s):  
Ultraviolet Radiation ◽  
Urocanic Acid ◽  
Monodelphis Domestica ◽  
Contact Hypersensitivity

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

1989 ◽  
Vol 170 (4) ◽  
pp. 1117-1131 ◽  
Author(s):  
L A Applegate ◽  
R D Ley ◽  
J Alcalay ◽  
M L Kripke
Keyword(s):  
Ultraviolet Radiation ◽  
Uv Irradiation ◽  
Langerhans Cells ◽  
Molecular Target ◽  
Monodelphis Domestica ◽  
Contact Hypersensitivity ◽  
Pyrimidine Dimer ◽  
Pyrimidine Dimers ◽  
Dorsal Epidermis ◽  
Epidermal Langerhans Cells

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.

A Critical Role for Dermal Mast Cells in Cis-Urocanic Acid-induced Systemic Suppression of Contact Hypersensitivity Responses in Mice

1999 ◽  
Vol 70 (5) ◽  
pp. 807-812 ◽  
Author(s):  
Prue H. Hart ◽  
Michele A. Grimbaldeston ◽  
Georgina J. Swift ◽  
Emma K. Hosszu ◽  
John J. Finlay-Jones
Keyword(s):  
Mast Cells ◽  
Critical Role ◽  
Urocanic Acid ◽  
Contact Hypersensitivity ◽  
In Cis

Enhancement of the Elicitation Phase of the Murine Contact Hypersensitivity Response by Prior Exposure to Local Ultraviolet Radiation

1986 ◽  
Vol 86 (1) ◽  
pp. 13-17 ◽  
Author(s):  
Luigi Polla ◽  
Randall Margolis ◽  
Claudia Goulston ◽  
John A. Parrish ◽  
Richard D. Granstein
Keyword(s):  
Ultraviolet Radiation ◽  
Prior Exposure ◽  
Contact Hypersensitivity ◽  
Hypersensitivity Response
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