Vitamin D receptor upregulation in alloreactive human T cells

Hum Immunol. 2012 Jul;73(7):693-8. doi: 10.1016/j.humimm.2012.04.019. Epub 2012 Apr 28.

Abstract

Vitamin D deficiency is adversely associated with diseases characterized by inflammation. The combination of the high incidence of vitamin D deficiency in patients undergoing allogeneic stem cell transplants (SCT) and the potential role of vitamin D deficiency in influencing graft-versus-host disease led us to further characterize the expression of VDR on alloreactive T cells. We hypothesized that vitamin D receptor expression may directly regulate alloreactive T cell responses. To overcome existing limitations in measuring VDR in bulk cellular populations, we developed a flow cytometric assay to measure cytoplasmic VDR in human T cells. Upon stimulation, VDR was expressed extremely early and exhibited sustained upregulation with chronic stimulation. VDR expression was also coupled to cytokine production, proliferation, and ERK1/2 phosphorylation. In addition, VDR exhibited a maturation stage-specific pattern of expression, with greatest expression on cells known to mediate GVHD, naïve and early memory T cells. Alloreactive T cells upregulated VDR, whereas the nonreactive T cells did not. Finally, repletion of vitamin D in vitro was sufficient to significantly reduce alloreactive T cell responses. These data suggest that vitamin D effects on T cells may be important in reducing graft versus host disease (GVHD) in the allogeneic stem cell transplant setting.

MeSH terms

  • Cell Differentiation
  • Cell Separation
  • Cells, Cultured
  • Flow Cytometry
  • Graft vs Host Disease / immunology*
  • Humans
  • Immunologic Memory
  • Immunomodulation
  • Isoantigens / immunology
  • Receptors, Calcitriol / genetics
  • Receptors, Calcitriol / metabolism*
  • Stem Cell Transplantation*
  • T-Lymphocyte Subsets / immunology
  • T-Lymphocyte Subsets / metabolism*
  • T-Lymphocytes / immunology
  • T-Lymphocytes / metabolism*
  • Up-Regulation
  • Vitamin D / metabolism

Substances

  • Isoantigens
  • Receptors, Calcitriol
  • Vitamin D