摘要：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.
