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Review
. 2008 Oct 1;105(2):338-43.
doi: 10.1002/jcb.21858.

Vitamin D and multiple sclerosis

Anita Raghuwanshi  1 , Sneha S Joshi, Sylvia Christakos
Affiliations
Review

Vitamin D and multiple sclerosis

Anita Raghuwanshi et al. J Cell Biochem. .

Abstract

Vitamin D is a principal regulator of calcium homeostasis. However, recent evidence has indicated that vitamin D can have numerous other physiological functions including inhibition of proliferation of a number of malignant cells including breast and prostate cancer cells and protection against certain immune mediated disorders including multiple sclerosis (MS). The geographic incidence of MS indicates an increase in MS with a decrease in sunlight exposure. Since vitamin D is produced in the skin by solar or UV irradiation and high serum levels of 25-hydroxyvitamin D (25(OH)D) have been reported to correlate with a reduced risk of MS, a protective role of vitamin D is suggested. Mechanisms whereby the active form of vitamin D, 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) may act to mediate this protective effect are reviewed. Due to its immunosuppressive actions, it has been suggested that 1,25(OH)(2)D(3) may prevent the induction of MS.

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Figures

Figure 1
Figure 1
Mechanism of repression of GM-CSF activated transcription by 1,25(OH)2D3. Unlike most mechanisms involved in 1,25(OH)2D3 mediated effects on transcription that require the VDR/RXR heterodimer, VDR bound to 1,25(OH)2D3 (VDRD3 in B) acts as a monomer on the GM-CSF promoter and competes with NFAT for binding to a composite NFAT AP1 site (composite site is shown in A). VDR bound to 1,25(OH)2D3 also stabilizes the binding of Fos-Jun heterodimer by direct interaction with cJun (B). These two events result in 1,25(OH)2D3 mediated transcriptional repression of GM-CSF (Adapted from Towers and Freedman, 1998)
See this image and copyright information in PMC

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