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Background  Vitamin D receptor (VDR) deficiency contributes to the development of experimental inflammatory bowel disease (IBD) in several different models. T cells have been shown to express the VDR, and T cells are targets of vitamin D. In this article we determined the effects of VDR expression on CD8 +  T cells.    Results  VDR KO CD8 +  T cells, but not WT CD8 +  T cells, induced colitis in Rag KO recipients. In addition, co-transfer of VDR KO CD8 +  T cells with naïve CD4 +  T cells accelerated colitis development. The more severe colitis was associated with rapidly proliferating naïve VDR KO CD8 +  T cells and increased IFN-γ and IL-17 in the gut. VDR KO CD8 +  T cells proliferated  in vitro  without antigen stimulation and did not downregulate CD62L and upregulate CD44 markers following proliferation that normally occurred in WT CD8 +  T cells. The increased proliferation of VDR KO CD8 +  cells was due in part to the higher production and response of the VDR KO cells to IL-2.    Conclusions  Our data indicate that expression of the VDR is required to prevent replication of quiescent CD8 +  T cells. The inability to signal through the VDR resulted in the generation of pathogenic CD8 +  T cells from rapidly proliferating cells that contributed to the development of IBD.

Vitamin D receptor expression controls proliferation of naïve CD8+ T cells and development of CD8 mediated gastrointestinal inflammation