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Department of Nutritional Sciences, Pennsylvania State University, University Park, Pennsylvania 16802
To whom requests for reprints should be addressed at 1 Department of Nutritional Sciences, 126 S. Henderson Building, Pennsylvania State University, University Park, PA 16802. E-mail: mxc69{at}psu.edu
Low vitamin D status has been implicated in the etiology of autoimmune diseases such as multiple sclerosis, rheumatoid arthritis, insulin-dependent diabetes mellitus, and inflammatory bowel disease. The optimal level of vitamin D intake required to support optimal immune function is not known but is likely to be at least that required for healthy bones. Experimentally, vitamin D deficiency results in the increased incidence of autoimmune disease. Mechanistically, the data point to a role for vitamin D in the development of self-tolerance. The vitamin D hormone (1,25-dihydroxy vitamin D3) regulates T helper cell (Th1) and dendritic cell function while inducing regulatory T-cell function. The net result is a decrease in the Th1-driven autoimmune response and decreased severity of symptoms. This review discusses the accumulating evidence pointing to a link between vitamin D and autoimmunity. Increased vitamin D intakes might decrease the incidence and severity of autoimmune diseases and the rate of bone fracture.
Key Words: vitamin D • autoimmunity • multiple sclerosis • arthritis • inflammatory bowel disease • insulin-dependent diabetes mellitus
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