Vitamin D 3 Suppresses Immune Reactions in Atherosclerosis, Affecting Regulatory T Cells and Dendritic Cell Function

Accumulated evidence indicates that 1,25-dihydroxyvitamin D3 (vitamin D3) plays important roles in bone and calcium metabolism and in immune processes.1–4 Several autoimmune disorders have been linked to a deficiency in vitamin D3.1–4 Epidemiological data indicate that vitamin D3 deficiency is associated with cardiovascular events.5,6See accompanying article on page 2495 In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology , Takeda et al7 report the results of a study undertaken to analyze the mechanisms by which vitamin D3 might affect the development of atherosclerotic lesions. By using a mouse model, Takeda et al demonstrated that an orally administered active form of vitamin D3 (calcitriol) led to a marked reduction in atherosclerotic lesion formation. The study revealed that a reduction in atherosclerotic lesion formation occurred by the suppression of immune reactions, with at least 2 cell types crucially involved in vitamin D3 effects (ie, CD4+CD25+ Fork head box protein [Foxp] 3+ regulatory T cells [Tregs] and dendritic cells [DCs]).Tregs exert functions in the induction and maintenance of immune tolerance.8–11 The family of Tregs is represented by a heterogeneous cell population that includes adaptive and naturally occurring Tregs.8–11 According to the current paradigm, adaptive Tregs develop from naive T cells in the periphery and can produce interleukin 10 and transforming growth factor β, whereas naturally occurring Tregs originate in …