Oral vitamin D increases the frequencies of CD38+ human B cells and ameliorates IL-17-producing T cells.

Vitamin D deficiency (serum 25-hydroxyvitamin D < 50 nm) has been associated with the onset of immunological diseases including atopic dermatitis (AD), cutaneous or systemic lupus erythematosus and allergic asthma. In this study, we assessed whether oral vitamin D (cholecalciferol) supplementation leads to a systemic modulation of the phenotype of circulating lymphocyte populations and whether a defined serum 25-hydroxyvitamin D (25(OH)D) concentration can be related to the effects on lymphocytes. Cholecalciferol was administered in a dose-escalation setting to vitamin D-deficient individuals from 2000 up to 8000 IU daily for 12 weeks. Individuals without cholecalciferol intake served as controls. Peripheral B cells and T cells were examined by multicolour flow cytometric analysis. The mean serum 25(OH)D concentrations increased upon cholecalciferol intake up to 159 ± 28.7 nm, and remained low in the control group 30.0 ± 12.5 nm. Following cholecalciferol intake, the frequencies of circulating CD38 expressing B cells were significantly increased and IFN-γ+ , and/or IL-17+ CD4+ T helper cells were decreased. These data were identified to correlate with the serum 25(OH)D levels by applying two different analysis approaches (ROC and a nonlinear regression analysis). Our data indicate that increasing 25(OH)D serum concentrations are associated with an increased expression of CD38 on B cells and a decreased T-cell-dependent proinflammatory cytokine production. The therapeutical role of our findings in systemic immunological diseases should be explored in the future by further controlled clinical studies.