New research has indicated that vitamin D directly terminates the production of a disease-causing protein, a discovery that may explain the association between levels of vitamin D in a person’s body and the person’s ability to resist or minimize the effects of MS.
According to the investigators, a collaborative team of scientists from the University of Medicine and Dentistry of New Jersey and Stanford University, the mechanism they identify suggests what might be a new path toward pharmaceutical treatment of MS, as well as therapies for other autoimmune diseases. The mechanism identified by the research team works like this:
During MS (“EAE” in mice), a damaging protein called interleukin-17 (IL-17) is produced by immune cells in the brain.
After vitamin D binds to its receptor, the receptor parks itself on the gene that encodes IL-17.
By doing so, the vitamin D receptor occupies a site normally reserved for a protein called NFAT, which is required to turn the IL-17 gene on.
The gene stays off and IL-17 levels plummet.
At the same time, the vitamin D receptor turns on another gene, whose product generates suppressive T cells that combat the destructive action of their IL-17-producing counterparts.
The study is published in the September issue of the journal Molecular and Cellular Biology.