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Oral vitamin D increases the frequencies of CD 38 + human B cells and ameliorates IL ‐17‐producing T cells
Author(s) -
Drozdenko Gennadiy,
Heine Guido,
Worm Margitta
Publication year - 2014
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.12300
Subject(s) - cholecalciferol , vitamin d and neurology , medicine , endocrinology , cd38 , cytokine , vitamin , t cell , immunology , vitamin d deficiency , immune system , biology , stem cell , cd34 , genetics
Vitamin D deficiency (serum 25‐hydroxyvitamin D < 50 n m ) 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 m , and remained low in the control group 30.0 ± 12.5 n m . Following cholecalciferol intake, the frequencies of circulating CD 38 expressing B cells were significantly increased and IFN ‐ γ + , and/or IL ‐17 + CD 4 + 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 CD 38 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.