myelin-oligodendrocyte-glycoprotein-(35-55) and Vitamin-D-Deficiency

The development of experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis, has been studied in mice that were (i) vitamin D-deficient, (ii) minus the vitamin D receptor, (iii) minus a vitamin D 25-hydroxylase, and (iv) minus the vitamin D 25-hydroxyvitamin D-1α-hydroxylase. EAE development was markedly suppressed in mice lacking the vitamin D receptor and partially suppressed in vitamin D-insufficient mice. However, the absence of either of the two key hydroxylases (i.e., 25-hydroxylase and 1α-hydroxylase) neither inhibits nor enhances the development of EAE. These results indicate that vitamin D and the vitamin D receptor are required for the development of EAE. The results also suggest that 1,25-dihydroxyvitamin D(3) may not play a role in this autoimmune response.

Topics: 25-Hydroxyvitamin D3 1-alpha-Hydroxylase; Animals; Body Weight; Calcium; Cholestanetriol 26-Monooxygenase; Disease Models, Animal; Encephalomyelitis, Autoimmune, Experimental; Female; Glycoproteins; Humans; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Myelin-Oligodendrocyte Glycoprotein; Peptide Fragments; Receptors, Calcitriol; Vitamin D; Vitamin D Deficiency