The Effects of Vitamin D on Immune System and Inflammatory Diseases

Abstract

Immune cells, including dendritic cells, macrophages, and T and B cells, express the vitamin D receptor and 1α-hydroxylase. In vitro studies have shown that 1,25-dihydroxyvitamin D, the active form of vitamin D, has an anti-inflammatory effect. Recent epidemiological evidence has indicated a significant association between vitamin D deficiency and an increased incidence, or aggravation, of infectious diseases and inflammatory autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis. However, the impact of vitamin D on treatment and prevention, particularly in infectious diseases such as the 2019 coronavirus disease (COVID-19), remains controversial. Here, we review recent evidence associated with the relationship between vitamin D and inflammatory diseases and describe the underlying immunomodulatory effect of vitamin D.

Keywords: COVID-19; immune system; multiple sclerosis (MS); rheumatoid arthritis (RA); systemic lupus erythematosus (SLE); vitamin D.

Figure 1

Effects of vitamin D on immune cells. Activation of toll-like receptors by pathogens increases the expression of vitamin D receptor (VDR) and CYP27B1. Upon entering the cell, 25D is metabolized to 1,25D by CYP27B1. 1,25D then binds to VDR, which induces cathelicidin and β-defensin 2. Cathelicidin promotes antibiotic activity via autophagy [14].

Figure 2

In experimental autoimmune encephalomyelitis (EAE) model, 1,25D inhibits interleukin (IL)-12 production by suppressing maturation of dendritic cells. Consequently, proliferation of Th1 cells is inhibited. On the other hand, 1,25D promotes the differentiation of T cells into Th2 or Treg cells. 1,25D plays an anti-inflammatory role by suppressing proinflammatory cytokines such as TNF-α or by promoting anti-inflammatory cytokines such as IL-10 or TGF-β derived from macrophages [27].