Vitamin D and the immune system

Abstract

It is now clear that vitamin D has important roles in addition to its classic effects on calcium and bone homeostasis. As the vitamin D receptor is expressed on immune cells (B cells, T cells, and antigen-presenting cells), and these immunologic cells are all capable of synthesizing the active vitamin D metabolite, vitamin D has the capability of acting in an autocrine manner in a local immunologic milieu. Vitamin D can modulate the innate and adaptive immune responses. Deficiency in vitamin D is associated with increased autoimmunity and an increased susceptibility to infection. As immune cells in autoimmune diseases are responsive to the ameliorative effects of vitamin D, the beneficial effects of supplementing vitamin D-deficient individuals with autoimmune disease may extend beyond the effects on bone and calcium homeostasis.

Figure 1

A. Effects of 1,25 Vitamin D on T cells include suppression of T cell proliferation, a shift from Th1 to a Th2 development, inhibition of Th17 cell development and facilitation of T regulatory cells. B. Effects of 1,25 Vitamin D on monocytes and dendric cells include inhibition of inflammatory cytokine production by monocytes and inhibition of dendritic cell differentiation and maturation.

Figure 2

A. Relative expression of 2 IFNα inducible genes, Mx1 and Ifit1 in SLE patients with vitamin D deficiency (≤ 20ng/ml) and sufficiency (>20ng/ml). Relative expression of these genes was determined by RTPCR on PBMCs from clinically stable SLE patients. Expression of interferon inducible genes is higher in patients with SLE with low serum vitamin D (unpublished data Ben-Zvi, I). B. Relative expression of 3 IFNα inducible genes (Mx1, Ifi1 and Ifit44) before and after (+D₃) supplementation with vitamin D₃ in 3 SLE patients. Vitamin D supplementation reduces expression of IFNα inducible genes (unpublished data Ben-Zvi, I).