| Autor: |
Xu, Chen, Poirier, Bruno, Duong Van Huyen, Jean-Paul, Lucchiari, Newton, Michel, Odile, Chevalier, Jacques, Kaveri, Srinivas |
| Zdroj: |
American Journal of Pathology; October 1998, Vol. 153 Issue: 4 p1257-1266, 10p |
| Abstrakt: |
Intravenous immunoglobulin (IVIg) is increasingly used in the treatment of autoimmune and inflammatory diseases, including vasculitides and Kawasaki disease. However, the outcome of IVIg interaction with endothelial cells of the vascular bed is not clear as yet. We have investigated the effect of IVIg on thein vitroactivation of human endothelial cells, as assessed by cell proliferation and reverse transcription-polymerase chain reaction-detected expression of mRNA coding for adhesion molecules (intercellular adhesion molecule-1 and vascular cellular adhesion molecule-1), chemokines (monocyte chemoattractant protein-1, macrophage colony-stimulating factor, and granulocyte-macrophage colony-stimulating factor), and proinflammatory cytokines (tumor necrosis factor-α, interleukin-1β, and interleukin-6). IVIg inhibited proliferation of endothelial cells in a time-dependent manner. This effect was dependent on both Fc and F(ab′)2fragments of the immunoglobulin molecule and was fully reversible. Tumor necrosis factor-α and interleukin-1β also inhibited thymidine incorporation, but to a lesser degree. IVIg had no effect on basal levels of mRNA coding for the adhesion molecules, chemokines, and proinflammatory cytokines. IVIg fully down-regulated the expression induced by tumor necrosis factor-α or interleukin-1β of mRNA coding for these molecules. Thus, blockade of cellular proliferation and of cytokine-induced expression of adhesion molecules, chemokines, and cytokines may explain the therapeutic effect of IVIg in vascular and inflammatory disorders. |
| Databáze: |
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