1alpha,25-Dihydroxyvitamin D(3) (1alpha,25(OH)(2)D(3)) and non-calcemic vitamin D analogs induce a persistent state of immaturity in dendritic cells both in vitro and in vivo. These effects are transcriptional in nature, involve alterations in surface ligands as well as cytokine synthesis and release, and are dependent upon the presence of the vitamin D receptor. The vitamin D endocrine system could also play a role in altering immune function in normal physiological conditions. Distinct differences exist in lymph node dendritic cells of vitamin D receptor null mutant mice when compared to normal mice.
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