Modulation of Monokine Production In Vitro by Human Intravenous Immunoglobulin
The mechanisms by which intravenous Ig acts in modulation of inflammatory diseases are unclear. One postulated effect operates by affecting cytokine production, interfering with ligand binding to interleukin (IL) receptors, or stimulating monocytes to IL-1 receptor antagonist release. In this study the attempt was made to elucidate whether the anti-pyretic effect of intravenous Ig in inflammatory conditions is caused by a direct suppression of monokine production. Mononuclear cells were isolated from healthy blood donors and stimulated with lipopolysaccharide (LPS) or Borrelia burgdorferi spirochetes (Bb) for induction of tumor necrosis factor-alpha (TNF-α), IL-1, and IL-6 in the absence or presence of intravenous Ig. The cytokine production was studied at a single cell level.
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