Abstract
BackgroundUltraviolet B irradiation confers strong resistance against experimental autoimmune encephalomyelitis, a model of multiple sclerosis. This protection by ultraviolet B is independent of vitamin D production but causes isomerization of urocanic acid, a naturally occurring immunosuppressant.MethodsTo determine whether UCA isomerization from trans to cis is responsible for the protection against experimental autoimmune encephalomyelitis afforded by ultraviolet B, trans- or cis-urocanic acid was administered to animals and their disease progression was monitored.ResultsDisease incidence was reduced by 74% in animals exposed to ultraviolet B, and skin cis-urocanic acid levels increased greater than 30%. However, increasing skin cis-urocanic acid levels independent of ultraviolet B was unable to alter disease onset or progression.ConclusionsIt is unlikely that urocanic acid isomerization is responsible for the ultraviolet B-mediated suppression of experimental autoimmune encephalomyelitis. Additional work is needed to investigate alternative mechanisms by which UVB suppresses disease.
Highlights
Ultraviolet B irradiation confers strong resistance against experimental autoimmune encephalomyelitis, a model of multiple sclerosis
EAE induction and scoring Mice were immunized at 9–10 weeks of age with myelin oligodendrocyte glycoprotein peptide (MOG)35–55 purchased from Hooke Laboratories (Lawrence, MA)
Under normal conditions, less than 1% of skin urocanic acid (UCA) content was in the cis form
Summary
Ultraviolet B irradiation confers strong resistance against experimental autoimmune encephalomyelitis, a model of multiple sclerosis. This protection by ultraviolet B is independent of vitamin D production but causes isomerization of urocanic acid, a naturally occurring immunosuppressant. Multiple sclerosis (MS), a demyelinating disease of the central nervous system, is less prevalent in locations that receive greater amounts of sunlight This observation has led to the hypothesis that vitamin D might play a major role in preventing the disease. Ultraviolet B (UVB) irradiation, especially the narrow band from 300 to 315 nm, confers resistance against EAE [9] This narrow band is exclusive of that required to generate vitamin D in the skin. UV light must confer protection by mechanisms distinct from vitamin D
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