rndsystems.com:

Multiple sclerosis (MS) is an autoimmune neurological disorder that affects over 2 million people worldwide. Onset of the disease is thought to occur following exposure of genetically predisposed individuals to an unknown environmental trigger that activates myelin-specific T cells. These cells cross the blood-brain barrier to trigger an inflammatory attack that demyelinates axons in the central nervous system.  Polymorphisms in the vitamin D receptor are among the genetic variations that increase the risk of MS. The incidence of MS is also elevated in northern climates, where vitamin D deficiency is common. Since exposure of the skin to ultraviolet light aids in the conversion of inactive vitamin D to the active form, the short days, low UV intensity, and lack of exposed skin common to winter months, decrease the amount of active VitD3 that can be produced. Although the correlation between VitD3 deficiency and MS is intriguing, we are only now beginning to understand the biology that may explain this connection. In both human MS and in experimental autoimmune encephalomyelitis (EAE), the mouse model of the disease, VitD3 can influence specialized populations of cells that may play a critical role in protection against the disease. VitD3 promotes the formation of tolerogenic or “semi-mature” dendritic cells (DCs). These DCs induce the development of CD25–FoxP3+/–IL-10++ Tr1 cells, a subset of regulatory T cells (Treg), and downregulate the production of Th1 inflammatory cells. A pair of interacting co-inhibitory proteins, B7-H1 (also known as PD-L1) and PD-1, appear to be critical molecules in this process.

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