Vitamin D Receptor (VDR) and Autoimmune Diseases

The vitamin_D_receptor (VDR) has great role in the regulates of expression of gene in several organs, responsive to vitamin D, after activation by physiologically active vit.D. There is strong evidence that vit.D is work in several physiological pathways, since vit.D-activating receptors and enzymes have been found in cell types that are unrelated to mineral and bone homeostasis. Many processes are affected by the so-called non-classic effects of VDR activation. These involve cell death, growth and reproduction of cells, and immune cell activity among many others. Moreover, immunity cells such as activated “CD4+ and CD8+ T cells, B cells, neutrophils, and antigen-presenting cells (APC) like dendritic cells and macrophages”, were found to have vitamin D receptors. Resting “T and B” lymphocytes express very little VDR, whereas dendritic cells and monocytes express it intracellularly. On the other side, VDR expression in T cells rises fivefold with lymphocyte activation. Variants in the VDR gene may have effect on susceptibility to endocrine auto-immune diseases. Among the most prevalent VDR polymorphisms, “TaqI, BsmI, ApaI, and FokI” have been investigated. The risk of autoimmune thyroid sickness (ATS) is highly correlated with the BsmI and TaqI polymorphism and the risk of systemic lupus erythematosus (SLE) is correlated with the BsmI and FokI polymorphism. The diabetic nephropathy may be affected by some VDR polymorphisms, such as FokI, while the risk of rheumatoid arthritis (RA) has been detected in the polymorphism of ApaI, BsmI, and TaqI. Vitamin D seems to be essential for immunological homeostasis, and research referred to the impact of this vitamin on the prevalence of autoimmune diseases.