Mechanism suggests a potential new path toward pharmaceutical treatment of MS, as well as therapies for other autoimmune diseases such as rheumatoid arthritis, type 1 diabetes, eczema and psoriasis.
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) but didn’t understood the mechanism involved. Until now.
New breakthrough research by a collaborative team at UMDNJ-New Jersey Medical School and Stanford indicates that vitamin D directly terminates the production of a disease-causing protein.
As the investigators outline in their report, published in the September issue of Molecular and Cellular Biology (“1,25-Dihydroxyvitamin D3 ameliorates Th17 autoimmunity via transcriptional modulation of interleukin-17A”):
• During MS (“EAE” in mice), a damaging protein called interleukin-17 (IL-17) is produced by immune cells in the brain.
• The research team found that 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.
According to the researchers, led by UMDNJ Prof. Sylvia Christakos, PhD, the mechanism they identified 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.
Source: UMDNJ news release, Aug 16, 2011