The calcitonin/calcitonin gene related peptide-α gene is not required for 1α,25-dihydroxyvitamin D₃-mediated suppression of experimental autoimmune encephalomyelitis

The active form of vitamin D, 1α,25-dihydroxyvitamin D₃ (1,25(OH)₂D₃), can suppress disease in the experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis. Calcium appears to be a critical component of 1,25(OH)₂D₃-mediated suppression of EAE, as complete disease prevention only occurs with a concomitant increase in serum calcium levels. Calcitonin (CT) is a peptide hormone released in response to acute increases in serum calcium, which led us to explore its importance in 1,25(OH)₂D₃-mediated suppression of EAE. Previously, we discovered that co-administration of pharmacological doses of CT enhanced the suppressive effect of 1,25(OH)₂D₃ on EAE, suggesting CT may play a role in 1,25(OH)₂D₃-mediated suppression of EAE. To determine the importance of CT in EAE we have utilized a mouse strain in which the gene encoding CT and its alternative splice product, calcitonin gene related peptide-α (CGRP), have been deleted. Deletion of the CT/CGRP gene had no effect on EAE progression. Furthermore, treatment with 1,25(OH)₂D₃ suppressed EAE in CT/CGRP knock-out mice equal to that in wild type mice. Therefore, we conclude that CT is not necessary for 1,25(OH)₂D₃-mediated suppression of EAE.