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Type 1 diabetes mellitus (T1DM) is an autoimmune disease, due to a large number of islet β cells damaged, resulting in an absolute lack of insulin, ultimately relying on insulin therapy. Vitamin D is a fat-soluble sterol derivative that not only participates in calcium and phosphorus metabolism but also acts as an immunomodulatory role by binding to nuclear vitamin D receptors to regulate the expression of transcription factors. Increasing evidence has shown that vitamin D has immunoregulation and anti-inflammatory effects, and it may play a role in T cell regulatory responses due to downregulation in the expression of cathepsin G and inhibition of CD4+ T cell activation and protection of β cells from immune attack and is beneficial in decreasing oxidative stress in T1DM patients. Epidemiologic evidence demonstrates involvement of vitamin D deficiency in T1DM pathogenesis, with the immune system improperly targeting and destroying its own islet β cells. In addition, polymorphisms in genes critical for vitamin D metabolism may increase the risk of islet autoimmunity and T1DM. In this paper, the relationship between vitamin D deficiency and the molecular mechanism of T1DM was discussed. [ABSTRACT FROM AUTHOR]

Type 1 diabetes (T1D) is an autoimmune disease mediated by T cells that selectively destroy the insulin-producing β cells. Previous reports based on epidemiological and animal studies have demonstrated that both genetic factors and environmental parameters can either promote or attenuate the progression of autoimmunity. In recent decades, several inbred rodent strains that spontaneously develop diabetes have been applied to the investigation of the pathogenesis of T1D. Because the genetic manipulation of mice is well developed (transgenic, knockout, and conditional knockout/transgenic), most studies are performed using the nonobese diabetic (NOD) mouse model. This paper will focus on the use of genetically manipulated NOD mice to explore the pathogenesis of T1D and to develop potential therapeutic approaches. [ABSTRACT FROM AUTHOR]