Diltiazem impairs maturation and functions of human dendritic cells

The aim of this study was to define the effects of diltiazem, a calcium antagonist drug used in cardiology and in clinical transplantation, on the differentiation and maturation of human dendritic cells (DC). Herein, we demonstrate that diltiazem, in association with granulocyte macrophage–colony-st...

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Bibliographic Details
Published in:Human immunology 2002-07, Vol.63 (7), p.524-533
Main Authors: Bachetoni, Alessandra, D’Ambrosio, Antonella, Mariani, Paola, Cortesini, Raffaello, Quintieri, Francesca
Format: Article
Language:English
Subjects:
Adjuvants, Immunologic - pharmacology
Cell Differentiation
Cells, Cultured
dendritic cells
Dendritic Cells - cytology
Dendritic Cells - drug effects
Dendritic Cells - immunology
diltiazem
Diltiazem - pharmacology
Down-Regulation
Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology
Humans
immunosuppressive drugs
Interleukin-12 - biosynthesis
Interleukin-4 - pharmacology
Monocytes - cytology
Monocytes - drug effects
Th1 Cells - drug effects
Th2 Cells - drug effects
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Summary:The aim of this study was to define the effects of diltiazem, a calcium antagonist drug used in cardiology and in clinical transplantation, on the differentiation and maturation of human dendritic cells (DC). Herein, we demonstrate that diltiazem, in association with granulocyte macrophage–colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4), induces monocytes to differentiate into cells with many of the characteristic of DC. However, diltiazem-induced DC express high levels of mannose receptor and FcγRII and, consequently, manifest a higher endocytic activity compared with GM-CSF+IL-4-induced DC. Importantly, diltiazem-induced DCs have an impaired responsiveness to lipopolysaccharide and CD40 ligand because they produce decreased levels of IL-12 and reveal a reduced ability to stimulate alloreactive T-cell responses as well as in inducing interferon-γ producing Th1 cells. These effects may contribute to a decreased DC-dependent T-cell activation and may help to explain the immunoregulatory function of diltiazem and its effectiveness in preventing transplant rejection.
ISSN:0198-8859
1879-1166
DOI:10.1016/S0198-8859(02)00407-X