Vitamin D pathway found for fighting MS
Vitamin D has been thought to play a role for battling multiple sclerosis, but scientists haven’t been sure exactly how. Researchers believe they may have discovered how the vitamin could combat the disease; potentially leading to new treatment.
Sylvia Christakos, Ph.D., of UMDNJ-New Jersey Medical School and colleagues seem to have honed in on the process that shows how vitamin D stops production of the damaging protein interleukin-17 (IL-17) that causes MS.
For the study, published in Molecular and Cellular Biology, researchers found vitamin D binds to IL-17 receptors produced by immune cells in the brain during MS. The researchers used mice with EAE - Experimental Allergic Encephalomyelitis (EAE) - a mouse model of multiple sclerosis
The research team, which included scientists from the University of Medicine and Dentistry of New Jersey and Stanford University, noted after vitamin D binds to the receptor, also blocks a protein called NFAT needed to turn on the gene. Without the gene “on”, levels of IL-17 fall.
Vitamin D also does another job by turning on a gene that produces suppressive T cells to fight destructive IL-17-production that occurs elsewhere.
According to the authors, in mouse models with EAE, vitamin D, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] “diminishes paralysis and progression of the disease and reduces IL-17A-secreting CD4+ T cells in the periphery and central nervous system (CNS).”
Identification of the vitamin D pathway could lead to new treatments not only for multiple sclerosis, but for other autoimmune diseases include type 1 diabetes, rheumatoid arthritis and skin disorders. The authors concluded, “Our results describe novel mechanisms and new concepts with regard to vitamin D and the immune system and suggest therapeutic targets for the control of autoimmune diseases.”
Molecular and Cellular Biology: doi:10.1128/MCB.05020-11
"1,25-Dihydroxyvitamin D3 Ameliorates Th17 Autoimmunity via Transcriptional Modulation of Interleukin-17A"
Sneha Joshi et al.;