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Received Jun 14, 2017; Accepted Aug 9, 2017
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1. Introduction
The main source of Vitamin D comes from sun exposure of the skin, from 7-dehidrocholesterol in response to ultraviolet B radiation (UVB), to further be metabolized in the liver to 25-hydroxyvitamin D 25(OH)D which is the metabolite used to assess vitamin D status. It requires further metabolism by the 1-alpha hydroxylase (CYP27B1) in the kidneys to produce the biologically active form 1,25-dihydroxyvitamin D (1,25(OH)2D3). In addition to the kidneys, many other tissues and cells throughout the body, including immune cells, express CYP27B1 and are therefore capable of regulating their own 1,25(OH)2D3 local concentration [1].
While the CYP27B1 in the kidneys is regulated by parathyroid hormone (PTH), fibroblast growth factor-23 (FGF-23), and 1,25(OH)2D3, its production in the immune system cells is driven by inflammatory conditions, either directly by the presence of cytokines [2] or in response to activation through the vitamin D receptor (VDR). Activated VDR binds response elements on DNA that are associated with antimicrobial [3] and immune regulatory functions [4]. Thus, vitamin D deficiency might result in the impaired function of immune cells [5] and cytokine imbalance [6, 7]. It has also been observed that sufficient 25(OH)D levels are related to increasing concentrations of IL-4 and IL-10 and to low levels of proinflammatory cytokines such as IL-1, IL-6, IL-12, IL-17, IL-23, and IFN-