The biologically active form of vitamin D, 1,25(OH)2D3, is a potent modulator of the immune system as well as a regulator of bone and mineral metabolism. Vitamin D-deficiency in infancy and vitamin D receptor gene polymorphisms may be risk factors for insulin-dependent Diabetes mellitus (IDDM). 1,25(OH)2D3 and its analogs significantly repress the development of insulitis and diabetes in the non-obese diabetic (NOD) mouse, a model of human IDDM. 1,25(OH)2D3 may modulate IDDM disease pathogenesis by repression of type I cytokines, inhibition of dendritic cell maturation, and upregulation of regulatory T cells. The function of vitamin D as a genetic and environmental determining factor for IDDM, the protective role of 1,25(OH)2D3 and its analogs in a mouse model of IDDM, and the possible mechanisms by which this protection occurs will be reviewed. © 2002 Wiley-Liss, Inc.
CITATION STYLE
Zella, J. B., & DeLuca, H. F. (2003). Vitamin D and autoimmune diabetes. In Journal of Cellular Biochemistry (Vol. 88, pp. 216–222). https://doi.org/10.1002/jcb.10347
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