Vitamin D does not modulate NF-κB activity in Jurkat T cells

Abstract

The active form of vitamin D, 1α,25-dihydroxyvitamin D 3 [1α,25(OH) 2D 3], has been reported to influence the functioning of the immune system by targeting the activities of cellular signaling pathways, in addition to its direct genomic effects. One of the signaling pathways reported to be targeted by vitamin D is the NF-κB pathway, which is highly active in most immune cell types, including T cells. However, the effects of vitamin D on the NF-κB pathway in T cells are not fully understood. Therefore, we examined the effects of 1α,25(OH) 2D 3 on the NF-κB pathway in the Jurkat cell line, a human T cell line that constitutively expresses endogenous vitamin D receptor. We found that 1α,25(OH) 2D 3 does not inhibit the induction of IκBα degradation and the expression of an NF-κB-dependent reporter gene in Jurkat cells following treatment with PMA/ionomycin. Also, 1α,25(OH) 2D 3 did not suppress the activation of NF-κB by TNFα or PHA. Furthermore, we demonstrate that 1α,25(OH) 2D 3 does not block the induction of CD69, which is an NF-κB target gene and an early T cell activation marker. Therefore, we conclude that vitamin D does not modulate the activity of the NF-κB pathway in Jurkat cells.