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Related Experiment Videos

1alpha,25-Dihydroxyvitamin D3 modulates CD38 expression on human lymphocytes

J D Stoeckler1, H A Stoeckler, N Kouttab

  • 1Department of Pathology, Roger Williams Medical Center and Brown University, Providence, RI 02908, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|December 1, 1996
PubMed
Summary

1alpha,25-dihydroxyvitamin D3 (1,25(OH)2D3) restores CD38 expression on stimulated B and T cells. This vitamin D3 analog up-regulates CD38 on lymphocytes, suggesting a role in immune cell regulation.

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Area of Science:

  • Immunology
  • Cell Biology
  • Endocrinology

Background:

  • CD38 is a cell surface glycoprotein expressed on various immune cells, including B and T lymphocytes.
  • Chronic stimulation can alter CD38 expression levels on lymphocytes.
  • 1alpha,25-dihydroxyvitamin D3 (1,25(OH)2D3) is the active form of vitamin D, known for its immunomodulatory effects.

Purpose of the Study:

  • To investigate the effect of 1,25(OH)2D3 on CD38 expression in chronically stimulated B cells and activated peripheral blood T cells.
  • To compare the efficacy of 1,25(OH)2D3 with other agents like all-trans-retinoic acid and interferons (IFNs) in modulating CD38 expression.

Main Methods:

  • In vitro culture of B cells from tonsils and peripheral blood T cells.
  • Stimulation of lymphocytes via CD40, antigen receptor, and PHA.

Related Experiment Videos

  • Treatment with 1,25(OH)2D3, all-trans-retinoic acid, IFNs, and IL-4.
  • Flow cytometry analysis to quantify CD38 expression and cell size.
  • Assessment of CD38 ectoenzyme activity in HL-60 cells.

    • Main Results:

    • 1,25(OH)2D3 restored CD38 expression on chronically stimulated B cells and upregulated it on CD38-/low cells.
    • 1,25(OH)2D3 significantly enhanced CD38 expression on activated peripheral blood T cells (CD8- and CD8+).
    • 1,25(OH)2D3 was more effective than all-trans-retinoic acid and showed differential effects compared to IFNs on B and T cells.
    • Hormonal induction of CD38 was linked to cell cycle entry, as indicated by cell size proportionality.
    • A delay in 1,25(OH)2D3's effect on lymphocytes suggested nuclear receptor upregulation, confirmed by rapid induction in HL-60 cells.

    Conclusions:

    • 1,25(OH)2D3 effectively modulates CD38 expression on both B and T lymphocytes.
    • The vitamin D metabolite's action on CD38 is cell-cycle dependent and involves nuclear receptors.
    • 1,25(OH)2D3 represents a potent agent for regulating CD38 expression in immune cells, with potential therapeutic implications.