UV radiation suppresses experimental autoimmune encephalomyelitis independent of vitamin D production

• Published in: Proceedings of the National Academy of Sciences - PNAS Vol. 107; no. 14; pp. 6418 - 6423
• Main Authors: Becklund, Bryan R, Severson, Kyle S, Vang, Souriya V, DeLuca, Hector F
• Format: Journal Article
• Language: English
• Published: United States National Academy of Sciences 06.04.2010; National Acad Sciences
• Subjects: Animals; Biological Sciences; Body Weight - radiation effects; Calcium; Calcium - blood; Disease models; Encephalomyelitis, Autoimmune, Experimental - immunology; Encephalomyelitis, Autoimmune, Experimental - metabolism; Encephalomyelitis, Autoimmune, Experimental - pathology; Epidemiology; Experimental autoimmune encephalomyelitis; Female; Genetics; Hypercalcemia; Hypercalcemia - blood; Hypercalcemia - etiology; Immune system; Immunization; Mice; Mice, Inbred C57BL; Multiple sclerosis; Sunlight; Ultraviolet radiation; Ultraviolet Rays; Vitamin D; Vitamin D - administration & dosage; Vitamin D - biosynthesis
• ISSN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.1001119107

Although the exact cause of multiple sclerosis (MS) is unknown, a number of genetic and environmental factors are thought to influence MS susceptibility. One potential environmental factor is sunlight and the subsequent production of vitamin D. A number of studies have correlated decreased exposure to UV radiation (UVR) and low serum 25-hydroxyvitamin D₃ [25(OH)D₃] levels with an increased risk for developing MS. Furthermore, both UVR and the active form of vitamin D, 1α,25-dihydroxyvitamin D₃, suppress disease in the experimental autoimmune encephalomyelitis (EAE) animal model of MS. These observations led to the hypothesis that UVR likely suppresses disease through the increased production of vitamin D. However, UVR can suppress the immune system independent of vitamin D. Therefore, it is unclear whether UVR, vitamin D, or both are necessary for the putative decrease in MS susceptibility. We have probed the ability of UVR to suppress disease in the EAE model of MS and assessed the effect of UVR on serum 25(OH)D₃ and calcium levels. Our results indicate that continuous treatment with UVR dramatically suppresses clinical signs of EAE. Interestingly, disease suppression occurs with only a modest, transient increase in serum 25(OH)D₃ levels. Further analysis demonstrated that the levels of 25(OH)D₃ obtained upon UVR treatment were insufficient to suppress EAE independent of UVR treatment. These results suggest that UVR is likely suppressing disease independent of vitamin D production, and that vitamin D supplementation alone may not replace the ability of sunlight to reduce MS susceptibility.