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Review
. 2015 Jul 27;7(8):6088-108.
doi: 10.3390/nu7085271.

Immune Modulation by Vitamin D and Its Relevance to Food Allergy

Affiliations
Review

Immune Modulation by Vitamin D and Its Relevance to Food Allergy

Noor H A Suaini et al. Nutrients. .

Abstract

Apart from its classical function in bone and calcium metabolism, vitamin D is also involved in immune regulation and has been linked to various cancers, immune disorders and allergic diseases. Within the innate and adaptive immune systems, the vitamin D receptor and enzymes in monocytes, dendritic cells, epithelial cells, T lymphocytes and B lymphocytes mediate the immune modulatory actions of vitamin D. Vitamin D insufficiency/deficiency early in life has been identified as one of the risk factors for food allergy. Several studies have observed an association between increasing latitude and food allergy prevalence, plausibly linked to lower ultraviolet radiation (UVR) exposure and vitamin D synthesis in the skin. Along with mounting epidemiological evidence of a link between vitamin D status and food allergy, mice and human studies have shed light on the modulatory properties of vitamin D on the innate and adaptive immune systems. This review will summarize the literature on the metabolism and immune modulatory properties of vitamin D, with particular reference to food allergy.

Keywords: 1,25(OH)2D3; T cells; adaptive immunity; deficiency; food allergy; inflammation; innate immunity; metabolism; vitamin D.

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Figures

Figure 1
Figure 1
Vitamin D metabolism and associated enzymes. Vitamin D from the diet and skin undergoes several hydroxylation steps to produce the biologically-active form of vitamin D, 1,25(OH)2D. In circulation, 1,25(OH)2D bound to the vitamin D binding protein (encoded by GC gene) is transported to the vitamin D target cells. Once it reaches the target cell, it dissociates from the binding protein and translocates to the nucleus, where it binds to the vitamin D receptor (VDR) and heterodimerizes with the retinoid X receptor (RXR). Recruitment of transcription factors results in the activation or repression of gene transcription. 1,25(OH)2D synthesis is regulated by feedback mechanisms involving fibroblast growth factor 23 (FGF-23) and parathyroid hormone (PTH). In the parathyroid gland, low serum calcium levels induce the secretion of PTH and activation of CYP27B1, resulting in the production of 1,25(OH)2D. As a second feedback loop, a high serum phosphate level triggers the secretion of FGF-23 from osteocytes and inhibits CYP27B1 synthesis. Activation of CYP24A1 also converts the bioactive vitamin D3 into inactive metabolites for secretion in bile.

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