The active form of vitamin D, 1α,25-dihydroxyvitamin D3 [1,25(OH)2D3], 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)2D3 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)2D3 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)2D3 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)2D3-mediated suppression of EAE
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