Vitamin D is a potent immune system regulator. The active form of vitamin D (1,25(OH)2D3) suppresses the development of animal models of human autoimmune diseases. 1,25(OH)2D3 decreased the proliferation of all T helper (h) cells and decreased the production of IFN-γ, IL-2, and IL-5. In Th2 cells 1,25(OH)2D3 increased the production of IL-4. Quiescent CD4+ T cells express vitamin D receptors but only at a low level, which increased five-fold following activation. 1,25(OH)2D3 treatment of Th0 cells, but not Th1 or Th2 cells, induced the expression of the transcription factor GATA-3. Microarray technology identified over 102 targets of 1,25(OH)2D3 in CD4+ T cells. Of the 102 genes, 57 genes were down-regulated and 45 were up-regulated by 1,25(OH)2D3 treatment of the CD4+ T cells. Two of the identified genes are regulators of NFkB. Other genes of interest included the IL-2Rβ gene and IgE binding factor. Th2 and Th0 cells produced more IgE binding factor after treatment with 1,25(OH)2D3 while Th1 cell IgE binding factor expression was unaffected by 1,25(OH)2D3 addition. It is unclear why some of the genes identified are expressed in CD4+ T cells and furthermore why 1,25(OH)2D3 regulates the expression of these genes. Clearly CD4+ T cells can be direct targets of vitamin D. The targets of vitamin D in CD4+ T cells depend on the state of activation and differentiation status of the cells. J. Cell. Biochem. 89: 922–932, 2003. © 2003 Wiley-Liss, Inc.
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