NEWARK, N.J.—Vitamin D, the principal regulator of calcium in the body, may prevent or minimize the effects of including multiple sclerosis (MS) by directly terminating the production of a disease-causing protein interleukin-17 (IL-17), according to a new study published in the journal Molecular and Cellular Biology.
During MS, IL-17 is produced by immune cells in the brain. Researchers at the University of Medicine and Dentistry of New Jersey and Stanford University found that that after vitamin D binds to its receptor, the receptor parks itself on the gene that encodes IL-17. The receptor then 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.
The researchers said the mechanism they identify may lead to 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.
