| [ Summary ] |
The relevance of the vitamin D3-vitamin D receptor (VDR) system to immunity remains unclear. However, dendritic cells, activated T cells, B cells, macrophages, rheumatoid synovial cells and many cells express VDR as a target for vitamin D3. Recent reports indicate the “non-calcemic” actions of VDR, which antagonize NF-AT or NF-κB-mediated transcription in immune cells. With these actions, vitamin D3 and its analogues are thought to induce tolerogenic dendritic cells and T cell anergy, in which there is an induction of antigen-specific regulatory T cells and conversion from Th1 to Th2-dominance. Therefore, these findings imply that VDR ligands could have a great potential for the development of therapies for autoimmune diseases and transplantation rejection. |