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

Abstract

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. 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). 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 CD38-HLA-DR+ subpopulations in both CD4+ and CD8+ T-cells, and decreased CD4+CD38-HLA-DR- and CD8+ CD38+HLA-DR+; whereas both calcidiol concentrations decreased the proliferation of CD38-HLA-DR- and CD38-HLA-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. 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.