Oral vitamin D increases the frequencies of CD38+ human B cells and ameliorates IL‐17‐producing T cells. Issue 2 (February 2014)

• Record Type: Journal Article
• Authors: Drozdenko, Gennadiy; Heine, Guido; Worm, Margitta
• Is Part Of: Experimental dermatology. Volume 23:Issue 2(2014:Feb.)
• Page Start: 107
• Page End: 112
• Publication Date: 2014-02
• Subjects: Dermatology -- Periodicals; 616.5
• DOI: 10.1111/exd.12300
• Languages: English
• ISSNs: 0906-6705

Abstract

<abstract abstract-type="main" id="exd12300-abs-0001"> <title>Abstract</title> <p>Vitamin D deficiency (serum 25‐hydroxyvitamin D < 50 n<sc>m</sc>) 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 n<sc>m</sc>, and remained low in the control group 30.0 ± 12.5 n<sc>m</sc>. Following cholecalciferol intake, the frequencies of circulating CD38 expressing B cells were significantly increased and IFN‐<italic>γ</italic><sup>+</sup>, and/or IL‐17<sup>+</sup> CD4<sup>+</sup> 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.</p> </abstract>