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01.12.2014 | Research article | Ausgabe 1/2014 Open Access

BMC Immunology 1/2014

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

Zeitschrift:
BMC Immunology > Ausgabe 1/2014
Autoren:
Jing Chen, Danny Bruce, Margherita T Cantorna
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1471-2172-15-6) contains supplementary material, which is available to authorized users.

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

JC, DB and MTC designed the research; JC and DB conducted the research; JC, DB and MTC analyzed the research; JC and MTC wrote the manuscript. MTC had primary responsibility for final content. All authors read and approved the final manuscript.

Abstract

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.
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