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Transcriptional Profiling of T Cells Identifies a Role for Vitamin D in the Immunoregulation of the V9V2 Response to Phosphate-Containing Ligands¹

Lanfen Chen^2,*, Maria Teresa Cencioni, Daniela F. Angelini, Giovanna Borsellino, Luca Battistini and Celia F. Brosnan^*

^* Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461; and Neuroimmunology Unit, Santa Lucia Foundation, Scientific Institute, Rome, Italy

Vitamin D is a steroid hormone that, in addition to its well-characterized role in calcium/phosphate metabolism, has been found to have regulatory properties for immune system function. The nuclear vitamin D receptor is widely expressed in tissues, but has also been shown to be regulated by hormones, growth factors, and cytokines. In this study we show that activation of human V2V9 T cells by nonpeptidic monoalkyl phosphates such as isopentenyl pyrophosphate leads to the up-regulation of the vitamin D receptor via a pathway that involves the classical isoforms of protein kinase C. We further show that this receptor is active by demonstrating that the ligand 1,25-dihydroxyvitamin D3 (vitD3) significantly inhibits in a dose-dependent fashion phospholigand-induced T cell expansion, IFN- production, and CD25 expression. We also show that vitD3 negatively regulates signaling via Akt and ERK and, at high concentrations, potentiates Ag-induced cell death. As such, these data provide further support for the immunoregulatory properties of vitamin D, and suggest that the ability of vitD3 to negatively regulate the proinflammatory activity of T cells may contribute to the protection this vitamin affords against inflammatory and autoimmune disorders dependent upon Th1-type responses.

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