Multiple Sclerosis (MS) is associated with vitamin D deficiency. This study examined some of the immunological effects of vitamin D on the prevention of MS in a mouse model. Pharmacologic targeting of T helper (TH) cell trafficking poses an attractive opportunity for amelioration of autoimmune diseases. The bioactive form of vitamin D, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], has been shown to prevent experimental autoimmune encephalomyelitis, a mouse model of MS, via an incompletely understood mechanism. In this study, the authors systematically examined 1,25(OH)2D3 effects on TH cells during their migration from the lymph nodes to the CNS. The results showed that myelin-reactive TH cells are successfully generated in the presence of 1,25(OH)2D3, secrete proinflammatory cytokines, and do not preferentially differentiate into suppressor T cells. These cells are able to leave the lymph node, enter the peripheral circulation, and migrate to the s.c. immunization sites. However, TH cells from 1,25(OH)2D3-treated mice are unable to enter the CNS parenchyma but are instead maintained in the periphery. Upon treatment cessation, mice rapidly develop experimental autoimmune encephalomyelitis, demonstrating that 1,25(OH)2D3 prevents the disease only temporarily likely by halting TH cell migration into the CNS. Proc Natl Acad Sci U S A, December 2013. PMID: 24324134
