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Author Information
Affiliations Department of Medicine and Pediatrics, Tulane School of Medicine, New Orleans, LA, USA Jay K. Kolls Department of Microbiology and Immunology, Tulane School of Medicine, New Orleans, LA, USA Robert F. Garry Authors Jay K. Kolls View author publications You can also search for this author in PubMed Google Scholar Robert F. Garry View author publications You can also search for this author in PubMed Google Scholar Corresponding author Correspondence to Jay K. Kolls. Rights and permissions Reprints and Permissions.
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He increasing prevalence of vitamin D deficiency and insufficiency and its association with an increased risk of autoimmune diseases and poor respiratory function, including asthma. These and additional studies have raised interest in the immunomodulatory properties of vitamin D beyond its well-established role in calcium homeostasis and bone health. This review discusses recent evidence that vitamin D promotes–both directly and indirectly–regulatory or suppressor T-cell populations with the capacity to inhibit inappropriate immune responses that cause disease, suggesting that this property may in part underpin the epidemiologic finding.
Introduction
Autoimmune diseases afflict ~50 million Americans and contribute >$100 billion to US health care costs (1). A deep understanding of disease mechanisms will be needed to deliver etiology-based strategies to reverse this vexing trend. Gene–environment interactions, sunlight and vitamin D, and T lymphocytes as autoimmune disease initiators and vitamin D targets are discussed to explain the rationale for reviewing vitamin D mechanisms in T cells.
Research on vitamin D regulation of thymocyte selection, Th1 and Th17 cells, T-cell programed cell death, and T-regulatory (Treg) cells is summarized and integrated into model mechanisms. Finally, unanswered questions relating to vitamin D mechanisms in CD4+ T cells are highlighted to promote further research that may lead to a deeper understanding of autoimmune disease molecular etiology.