Vitamin D in Systemic Lupus Erythematosus

Diane Kamen; Cynthia Aranow


Curr Opin Rheumatol. 2008;20(5):532-537. 

In This Article

Dendritic Cells

Vitamin D has profound effects on dendritic cells. Dendritic cells have important functions in maintaining both protective immunity and self-tolerance,[17,18] as immature dendritic cells promote T cell tolerance, whereas mature dendritic cells activate nave T cells. Mechanisms of action of vitamin D on dendritic cells include actions on the differentiation of monocytes into immature dendritic cells, the maturation of dendritic cells and dendritic cell survival.[19,20,21,22,23] Physiologic levels of 1,25D inhibit the maturation of dendritic cells and maintain an immature phenotype with inhibition of activation markers such as major histocompatibility complex (MHC) class II, CD40, CD80 and CD 86.[19] Furthermore, 1,25D downregulates dendritic cell production of IL-12 and augments IL-10.[9] Dendritic cells that have differentiated from monocytes (MDDCs) in the presence of 1,25D are immature and exhibit less IL-12p40 levels in response to lipopolysaccharide (a maturation trigger for immature dendritic cells). They also respond poorly to inflammatory chemokines that regulate dendritic cell migration to lymph nodes.[21] As the maturational state of dendritic cells can be modulated by vitamin D, the vitamin D status of an individual is likely to have important consequences in autoimmune conditions.

Importantly, we have shown that MDDCs from patients with SLE behave similarly as MDDCs from normal individuals when exposed to physiologic concentrations of vitamin D. SLE MDDCs differentiated in vitamin D maintain an immature phenotype with inhibited expression of human leukocyte antigen-DR (HLADR), CD40 and CD86 (unpublished data).


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