Abstract
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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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25-Hydroxyvitamin D3 1-alpha-Hydroxylase / genetics
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25-Hydroxyvitamin D3 1-alpha-Hydroxylase / metabolism*
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Animals
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Body Weight
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Calcium / administration & dosage
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Calcium / blood
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Calcium / metabolism
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Cholestanetriol 26-Monooxygenase / genetics
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Cholestanetriol 26-Monooxygenase / metabolism*
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Disease Models, Animal
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Encephalomyelitis, Autoimmune, Experimental / genetics
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Encephalomyelitis, Autoimmune, Experimental / immunology
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Encephalomyelitis, Autoimmune, Experimental / metabolism*
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Female
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Glycoproteins / immunology
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Humans
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Male
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Myelin-Oligodendrocyte Glycoprotein
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Peptide Fragments / immunology
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Receptors, Calcitriol / genetics
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Receptors, Calcitriol / metabolism*
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Vitamin D / administration & dosage
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Vitamin D / blood
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Vitamin D / metabolism*
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Vitamin D Deficiency / blood
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Vitamin D Deficiency / metabolism
Substances
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Glycoproteins
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Myelin-Oligodendrocyte Glycoprotein
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Peptide Fragments
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Receptors, Calcitriol
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myelin oligodendrocyte glycoprotein (35-55)
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Vitamin D
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Cyp2r1 protein, mouse
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Cholestanetriol 26-Monooxygenase
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25-Hydroxyvitamin D3 1-alpha-Hydroxylase
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Calcium