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From the Unité de Recherche "Immunopathologie Humaine," INSERM U430, and Claude Bernard Association, Hôpital Broussais, Paris, France
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 the
in vitro activation 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-
,
interleukin-1ß, and interleukin-6). IVIg inhibited
proliferation of endothelial cells in a time-dependent manner. This
effect was dependent on both Fc and F(ab')2 fragments of
the immunoglobulin molecule and was fully reversible. Tumor necrosis
factor- and interleukin-1ß 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- or
interleukin-1ß 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.
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