While for years scientists have noted an association between levels of vitamin D in a person's body and the person's ability to resist or minimize the effects of multiple sclerosis (MS), the mechanism involved has not been established. However new research by Sylvia Christakos, Ph.D., of UMDNJ-New Jersey Medical School (principal investigator) Sneha Joshi (first author, a UMDNJ Ph.D. student), and colleagues (including co-investigator Lawrence Steinman, MD, of Stanford University) appears to have uncovered that process. The study, published in the journal Molecular and Cellular Biology, finds that vitamin D directly terminates the production of a disease-causing protein.
During MS ("EAE" in mice), a damaging protein called interleukin-17 (IL-17) is produced by immune cells in the brain. The investigators, a collaborative team of scientists from the University of Medicine and Dentistry of New Jersey and Stanford University, find that after vitamin D binds to its receptor, the receptor parks itself on the gene that encodes IL-17. By doing so, the receptor occupies a site normally reserved for a protein called NFAT, which is required to turn the 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.
According to the researchers, the mechanism they identify suggests what might be a new path toward pharmaceutical treatment of MS, as well as therapies for other autoimmune diseases that might include rheumatoid arthritis, type 1 diabetes, eczema and psoriasis.