Ultraviolet-irradiated urocanic acid suppresses delayed-type hypersensitivity to herpes simplex virus in mice.
Ultraviolet radiation is known to induce a transient defect in epidermal antigen presentation which leads to the generation of antigen-specific suppression of the delayed-type hypersensitivity (DTH) response. The putative receptor in skin for the primary event in UV-suppression is urocanic acid (UCA) which may then interact locally, or systemically, with antigen presenting cells or initiate a cascade of events resulting in suppression. We present the first direct evidence that UCA, when irradiated with a dose (96 mJ/cm2) of UVB radiation known to suppress the DTH response to herpes simplex virus, type 1 (HSV-1) in mice, can induce suppression following epidermal application or s.c. injection of the irradiated substance. This suppression is transferable with nylon wool-passed spleen cells.
D000818:Animals; D000956:Antigens, Viral / Q000276:immunology; D006968:Hypersensitivity, Delayed / Q000276:immunology*; D007093:Imidazoles / Q000276:immunology*; D007108:Immune Tolerance; D007111:Immunity, Cellular / Q000187:drug effects / Q000528:radiation effects*; D051379:Mice; D018139:Simplexvirus / Q000276:immunology; D013154:Spleen / Q000276:immunology; D013237:Stereoisomerism; D014466:Ultraviolet Rays; D014560:Urocanic Acid / Q000031:analogs & derivatives / Q000276:immunology*
D000956:Antigens, Viral; D007093:Imidazoles; D014560:Urocanic Acid