Vitamin D deficiency diminishes the severity and delays onset of experimental autoimmune encephalomyelitis

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• 作者：Hector F. DeLuca  ; ;   ; ^{deluca@biochem.wisc.edu} ;   ; ^{mings@biochem.wisc.edu} ; Lori A. Plum
• 关键词：Multiple sclerosis ; Autoimmune disease ; Paralysis ; Vitamin D function
• 刊名：Archives of Biochemistry and Biophysics
• 出版年：2011
• 出版时间：15 September 2011
• 年：2011
• 卷：513
• 期：2
• 页码：140-143
• 全文大小：334 K

文摘

Multiple sclerosis incidence is clearly inversely related to sun exposure. This observation led to the idea that vitamin D might be responsible for this relationship. Providing super-physiologic doses of the hormonal form of vitamin D, 1¦Á,25-dihydroxyvitamin D₃, suppresses an animal model of multiple sclerosis, i.e. experimental autoimmune encephalomyelitis (EAE) but causes unwanted hypercalcemia. Further, dietary calcium is needed for this activity of 1¦Á,25-dihydroxyvitamin D₃. B10PL mice were maintained on a vitamin D-deficient diet for two generations to produce frank vitamin D deficiency. These animals showed delayed onset and reduced severity of EAE compared to control animals on the same diet and given vitamin D₃ or provided a vitamin D-containing chow diet. Thus, vitamin D deficiency interferes with the development of this autoimmune disease rather than increasing susceptibility.