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Human dendritic cells (DC) can be differentiated from blood monocytes in the presence of GM-CSF and IL-4 and matured by lipopolysaccharide (LPS). Vitamin D 3  inhibits the maturation of human DC measured by changes in surface expression of HLA-DR, CD14, CD40, CD80, CD83, and CD86. We here examine the function of vitamin D 3  during DC maturation. One of the earliest changes to LPS-induced maturation was an increase in CD83 expression. Vitamin D 3  inhibited the increase in expression of HLA-DR, CD40, CD80, CD83, and CD86 and the decrease in expression of CD14, which was paralleled morphologically by vitamin D 3 -induced inhibition of dendritic cell differentiation. Vitamin D 3  acted in synergy with the TLR agonists LPS and peptidoglycan (PGN) in inducing IL-6, IL-8, and IL-10, whereas vitamin D 3  completely inhibited LPS-induced secretion of IL-12. The synergy occurred at concentrations where neither vitamin D 3  nor the TLR agonists alone induced measurable cytokine secretion. Both LPS and PGN enhanced the level of the vitamin D 3  receptor (VDR). Taken together, these data demonstrated that vitamin D 3  and TLR agonists acted in synergy to alter secretion of cytokines from human DC in a direction that may provide an anti-inflammatory environment.

Synergy between Vitamin D3and Toll-Like Receptor Agonists Regulates Human Dendritic Cell Response during Maturation

Synergy between Vitamin D₃and Toll-Like Receptor Agonists Regulates Human Dendritic Cell Response during Maturation