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Licensed Unlicensed Requires Authentication Published by De Gruyter February 21, 2017

Vitamin D modulates the expression of HLA-DR and CD38 after in vitro activation of T-cells

  • Simon Villegas-Ospina , Wbeimar Aguilar-Jimenez , Sandra M. Gonzalez and María T. Rugeles EMAIL logo

Abstract

Objective:

Vitamin D (VitD) is an anti-inflammatory hormone; however, some evidence shows that VitD may induce the expression of activation markers, such as CD38 and HLA-DR. We explored its effect on the expression of these markers on CD4+ and CD8+ T-cells in vitro, and their potential correlations in vivo.

Materials and methods:

CD38 and HLA-DR expression was measured by flow cytometry in PHA/IL-2-activated mononuclear cells cultured under VitD precursors: three cholecalciferol (10−11M, 10−9M, 10−7M; n=11) and two calcidiol (40 ng/mL, 80 ng/mL; n=9) concentrations. The correlation between the expression of these markers in freshly isolated blood cells and serum levels of calcidiol was also explored (n=10).

Results:

Cholecalciferol at 10−7M increased the proportion of CD4+ CD38+ and CD8+ CD38+ cells, and decreased CD8+HLA-DR+ cells. As co-expression, it increased the CD38+HLA-DR and decreased CD38HLA-DR+ subpopulations in both CD4+ and CD8+ T-cells, and decreased CD4+CD38HLA-DR and CD8+ CD38+HLA-DR+; whereas both calcidiol concentrations decreased the proliferation of CD38HLA-DR and CD38HLA-DR+ subpopulations. Both forms of VitD increased the number of CD38 molecules per cell. In contrast, there was a positive but non-significant correlation between serum calcidiol levels and the expression of CD38 and HLA-DR in CD4+ and CD8+ T-cells.

Conclusion:

Although no significant correlations were observed in vivo in healthy subjects, VitD treatment in vitro modulated immune activation by increasing the expression of CD38 and decreasing the proliferation of HLA-DR+ and resting cells, which may correlate with improved effector and decreased proliferative capabilities. These results highlight the potential use of VitD as therapeutic strategy in immune disorders.

Acknowledgments

The authors thank the volunteers who kindly participated in this study and to Ana L. Rodriguez and Paula Velilla for their support in flow cytometry analysis.

  1. Author Statement

  2. Research funding: This investigation was supported by Colciencias 111565740508 and by Universidad de Antioquia UdeA (Sostenibilidad and CODI, act 2014-938). WAJ is recipient of a doctoral scholarship from Colciencias. The funders had no role in study design, data collection and analyses, decision to publish, or preparation of the manuscript.

  3. Conflict of interest: Authors state no conflict of interest.

  4. Informed consent: Informed consent has been obtained from all individuals.

  5. Ethical approval: The research related to human use complied with all the relevant national regulations and institutional policies and was performed in accordance to the tenets of the Helsinki Declaration and has been approved by the author’s institutional review board or equivalent committee.

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Supplemental Material:

The online version of this article (DOI: 10.1515/hmbci-2016-0037) offers supplementary material, available to authorized users.


Received: 2016-7-17
Accepted: 2016-12-29
Published Online: 2017-2-21
Published in Print: 2017-3-1

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