Vitamin D in Systemic Lupus Erythematosus

Diane Kamen; Cynthia Aranow


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

In This Article

T and B Cells

Quiescent CD4 T lymphocytes express the VDR and upregulate its expression fivefold upon activation.[1] Vitamin D suppresses T cell receptor-induced T cell proliferation[2,3] and specifically appears to inhibit Th1 cell proliferation.[4,5] Interferon-gamma (IFN?) and interleukin (IL)-2 production by T cells is diminished by exposure to 1,25D, whereas IL-5 and IL-10 are increased, consistent with a shift towards a Th2 response.[6,7] The production of the Th2 cytokine IL-4 is upregulated by vitamin D in most but not all studies.[6,8] Vitamin D appears to directly inhibit Th1 cells and may additionally modulate a skewing towards a Th2 response by its inhibitory effects upon IL-12 (IL-12 promotes a Th1 CD4 cell response).[9] In addition to effects of CD4 cells, vitamin D facilitates the induction of Foxp3+ T regulatory cells.[10,11] There have been no published studies examining the direct effects of vitamin D on Th17 cells; however, vitamin D inhibits the expression of IL-6,[12,13] a cytokine that stimulates Th17 genesis. Vitamin D has a direct effect on B cells and inhibits immunoglobulin production.[14] Furthermore, when exposed in vitro to vitamin D, differentiation of B lymphocytes is interrupted.[15] Peripheral blood mononuclear cells (PBMCs) from patients with SLE are sensitive to the effects of vitamin D; addition of vitamin D to SLE PBMCs results in a significant reduction of both spontaneous polyclonal antibody production and antidsDNA autoantibody production by SLE B cells.[16]


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