Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 106, Issue 13, Pages 5276-5281Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0813312106
Keywords
calcium; calcium homeostasis; immune system; multiple sclerosis; vitamin D
Categories
Funding
- Wisconsin Alumni Research Foundation
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The active form of vitamin D, 1 alpha,25-dihydroxyvitamin D-3 [1,25(OH)(2)D-3], suppresses disease development in the experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis (MS). However, complete disease prevention only occurs with doses that dramatically elevate serum calcium levels, thus limiting the usefulness of 1,25(OH)(2)D-3 as a potential MS therapeutic agent. Because calcitonin (CT) is believed to be released by hypercalcemia and has been shown to be anti-inflammatory, we examined whether suppression of EAE by 1,25(OH)(2)D-3 could be mediated either in part or entirely by CT. Continuous administration of pharmacological doses of CT did not prevent EAE. However, a combination of CT and a subtherapeutic dose of 1,25(OH)(2)D-3 additively suppressed EAE without causing hypercalcemia. Moreover, CT decreased the dose of 1,25(OH)2D3 required for disease suppression. Our results suggest that CT may be a significant factor but cannot account entirely for 1,25(OH)(2)D-3-mediated suppression of EAE.
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