Proceedings of the National Academy of Sciences · 2012 · 59 citations · 20 references
Life SciencesImmunologyNeuroscienceAutoimmunityImmunopathologyNeuroimmunologyAutoimmune DiseasesDemyelinating DiseasesMultiple SclerosisVitamin DVitamin D DeficiencyVitamin D MetabolismExperimental Autoimmune EncephalomyelitisMultiple Sclerosis PathologyVitamin D HomeostasisVitamin D InsufficiencyVitamin D PhysiologyVitamin D Receptor SignalingVitamin D ReceptorsVitamin D Sufficiency
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.
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