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Background  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.    Methods  To 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.    Results  Disease 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.    Conclusions  It 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.

Suppression of experimental autoimmune encephalomyelitis by ultraviolet light is not mediated by isomerization of urocanic acid