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

BMC Neuroscience

Research Article

Steven J. Marling¹  Lori A. Plum¹  Hector F. DeLuca¹  Amy A. Irving¹ 

[1] Department of Biochemistry, University of Wisconsin-Madison, 433 Babcock Drive, 53706, Madison, WI, USA;

关键词: Multiple Sclerosis;    Experimental Autoimmune Encephalomyelitis;    Trans Isomer;    Myelin Oligodendrocyte Glycoprotein;    Spleen Weight;   

DOI  :  10.1186/s12868-016-0323-2

 received in 2016-08-03, accepted in 2016-12-14,  发布年份 2017

来源: Springer

【 摘 要 】

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.

【 授权许可】

CC BY   
© The Author(s) 2017