Cantorna Margherita T, Mahon Brett D
Department of Nutritional Sciences, Pennsylvania State University, University Park, PA 16802, USA.
Exp Biol Med (Maywood). 2004 Dec;229(11):1136-42. doi: 10.1177/153537020422901108.
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 D(3)) 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.
低维生素D状态与自身免疫性疾病的病因有关，如多发性硬化症、类风湿性关节炎、胰岛素依赖型糖尿病和炎症性肠病。支持最佳免疫功能所需的最佳维生素D摄入量尚不清楚，但可能至少是维持健康骨骼所需的量。在实验中，维生素D缺乏会导致自身免疫性疾病发病率增加。从机制上讲，数据表明维生素D在自身耐受的发展中起作用。维生素D激素（1,25-二羟基维生素D3）调节辅助性T细胞（Th1）和树突状细胞功能，同时诱导调节性T细胞功能。最终结果是Th1驱动的自身免疫反应减少，症状严重程度降低。本文综述了越来越多的证据，表明维生素D与自身免疫之间存在联系。增加维生素D摄入量可能会降低自身免疫性疾病的发病率和严重程度以及骨折发生率。
