| First Author | Chen J | Year | 2014 |
| Journal | BMC Immunol | Volume | 15 |
| Pages | 6 | PubMed ID | 24502291 |
| Mgi Jnum | J:323210 | Mgi Id | MGI:6871937 |
| Doi | 10.1186/1471-2172-15-6 | Citation | Chen J, et al. (2014) Vitamin D receptor expression controls proliferation of naive CD8+ T cells and development of CD8 mediated gastrointestinal inflammation. BMC Immunol 15:6 |
| abstractText | 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 naive CD4+ T cells accelerated colitis development. The more severe colitis was associated with rapidly proliferating naive VDR KO CD8+ T cells and increased IFN-gamma 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. |
