Vitamin D Actions on CD4+ T Cells in Autoimmune Disease

This review summarizes and integrates research on vitamin D and CD4+ T-lymphocyte biology to develop new mechanistic insights into the molecular etiology of autoimmune disease

Colleen Elizabeth Hayes

2015

Scholarcy highlights

  • Autoimmune diseases afflict ~50 million Americans and contribute >$100 billion to US health care costs
  • Cell culture studies have shown that adding calcitriol to www.frontiersin.org some human in vivo data that are consistent with animal modeling, it is reasonable to suggest that vitamin D may significantly influence the emergence of an autoimmune disease phenotype by dampening pathogenic Th17 cells and IL-17 synthesis
  • RESEARCH DIRECTIONS This review article sought to summarize and integrate research on vitamin D and CD4+ T-lymphocyte biology in an effort to develop a new understanding of the molecular etiology of autoimmune disease
  • There is a large, latitude-linked, non-transmissible environmental component that acts at the population level to determine the emergence of an autoimmune phenotype, given an autoimmune disease-susceptible genotype
  • Diverse and compelling evidence suggests that this environmental component is ambient UVB light exposure catalyzing cutaneous vitamin D3 formation
  • The strength and universality of ambient UVB light and vitamin D3 as autoimmune disease risk factors, the vitamin D hormone’s established role as a transcriptional regulator of gene expression, and the role of CD4+ T lymphocytes as autoimmune disease initiators and suppressors provided the rationale for closely examining calcitriol regulation of CD4+ T-lymphocyte function in this review
  • This evidence has contributed to a greater functional and mechanistic understanding of the molecular etiology of autoimmune disease, one of the major challenges in modern immunobiology

Need more features? Save interactive summary cards to your Scholarcy Library.