Vitamin d as an immune system regulator: Inhibiton of experimental autoimmune encephalomyelitis

Historically, vitamin D has been associated with mineral metabolism regulation. Here we show that vitamin D reversibly inhibited the progression of murine experimental autoimmune encephalomyelitis (EAE), a T cell-mediated autoimmune disease that serves as a model for multiple sclerosis. Myelin basic protein (MBP) immunized mice were given an intraperitoneal injection of vitamin D diluted in PBS or PBS only, at the time that EAE symptoms were first detectable (6-10 days postimmunization). Vitamin D treatments stopped the progression of EAE in these mice. When vitamin D was then removed from the diet of the vitamin D-treated mice, the severity of their EAE increased to that of untreated controls. This suggests that vitamin D suppression was reversible, having rendered the autoimmune T cells temporarily anergic. Vitamin D treatment in vivo during MBP priming resulted in a lowered Th 1 cell frequency (compared to controls), and the generation of Th2 cells, which were absent in the control animals. Furthermore, vitamin D treatment of adherent peritoneal exudate cells in vitro markedly increased TGF-β gene transcription. Thus, vitamin D is a critically important immune system regulator and possibly a treatment for multiple sclerosis.