» Articles » PMID: 20308557

UV Radiation Suppresses Experimental Autoimmune Encephalomyelitis Independent of Vitamin D Production

Overview
Specialty Science
Date 2010 Mar 24
PMID 20308557
Citations 82
Authors
Affiliations
Soon will be listed here.
Abstract

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 D(3) [25(OH)D(3)] levels with an increased risk for developing MS. Furthermore, both UVR and the active form of vitamin D, 1alpha,25-dihydroxyvitamin D(3), 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)D(3) 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)D(3) levels. Further analysis demonstrated that the levels of 25(OH)D(3) 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.

Citing Articles

Illuminating the Connection: Cutaneous Vitamin D Synthesis and Its Role in Skin Cancer Prevention.

Ucar N, Holick M Nutrients. 2025; 17(3).

PMID: 39940244 PMC: 11821240. DOI: 10.3390/nu17030386.


Advanced and Metastatic Non-Melanoma Skin Cancer: Epidemiology, Risk Factors, Clinical Features, and Treatment Options.

Attal Z, Shalata W, Soklakova A, Tourkey L, Shalata S, Abu Saleh O Biomedicines. 2024; 12(7).

PMID: 39062023 PMC: 11274597. DOI: 10.3390/biomedicines12071448.


Association between sun exposure habits and disease progression in multiple sclerosis.

Wu J, Olsson T, Alfredsson L, Hedstrom A Eur J Neurol. 2024; 31(6):e16269.

PMID: 38440929 PMC: 11235876. DOI: 10.1111/ene.16269.


Risk factors for multiple sclerosis in the context of Epstein-Barr virus infection.

Hedstrom A Front Immunol. 2023; 14:1212676.

PMID: 37554326 PMC: 10406387. DOI: 10.3389/fimmu.2023.1212676.


Association of Latitude and Exposure to Ultraviolet B Radiation With Severity of Multiple Sclerosis: An International Registry Study.

Vitkova M, Diouf I, Malpas C, Horakova D, Kubala Havrdova E, Patti F Neurology. 2022; 98(24):e2401-e2412.

PMID: 35410900 PMC: 9231838. DOI: 10.1212/WNL.0000000000200545.


References
1.
Sutherland J, Tyrer J, Eadie M . The prevalence of multiple sclerosis in Australia. Brain. 1962; 85:149-64. DOI: 10.1093/brain/85.1.149. View

2.
FISHER M, Kripke M . Systemic alteration induced in mice by ultraviolet light irradiation and its relationship to ultraviolet carcinogenesis. Proc Natl Acad Sci U S A. 1977; 74(4):1688-92. PMC: 430858. DOI: 10.1073/pnas.74.4.1688. View

3.
Deluca H . Overview of general physiologic features and functions of vitamin D. Am J Clin Nutr. 2004; 80(6 Suppl):1689S-96S. DOI: 10.1093/ajcn/80.6.1689S. View

4.
Jones G, Strugnell S, DeLuca H . Current understanding of the molecular actions of vitamin D. Physiol Rev. 1998; 78(4):1193-231. DOI: 10.1152/physrev.1998.78.4.1193. View

5.
Lemire J, Archer D . 1,25-dihydroxyvitamin D3 prevents the in vivo induction of murine experimental autoimmune encephalomyelitis. J Clin Invest. 1991; 87(3):1103-7. PMC: 329907. DOI: 10.1172/JCI115072. View