1,25-Dihydroxyvitamin D suppressed experimental autoimmune encephalomyelitis through both immunomodulation and oligodendrocyte maturation.

1,25-Dihydroxyvitamin D (1,25(OH)D) has recently been found to have the anti-inflammatory potential to suppress experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis; however, its direct effect on neural cells is not clear. In the current study we show that 1,25(OH)D treatment effectively suppressed clinical signs of ongoing EAE and reduced inflammation and demyelination scores in the central nervous system (CNS). The treatment significantly decreased production/expression of pro-inflammatory cytokines IFN-γ, GM-CSF and IL-17A, while it increased anti-inflammatory cytokines IL-4 and IL-10. Further, 1,25(OH)D treatment effectively elevated the numbers of neural stem cells, oligodendrocyte precursor cells, as well as oligodendrocytes in disease lesions in the CNS. These results, together with its in vitro effect of inducing oligodendrocyte differentiation as shown in our previous findings, demonstrate that 1,25(OH)D suppressed EAE not only by its immunomodulatory capacity, but also by its effect on oligodendrocyte differentiation and maturation, and thus has potential for remyelination and neural repair.