Intravenous immunoglobulin G (IVIG) inhibits IL-1- and TNF-α-dependent, but not chemotactic-factor-stimulated, neutrophil transendothelial migration.

High-dose intravenous immunoglobulin (IVIG) has anti-inflammatory effects via incompletely understood mechanisms. By investigating whether IVIG might modulate neutrophil (PMN) recruitment, we observed that IVIG dose-dependently inhibited (by 30-50%) PMN transendothelial migration (TEM) across human umbilical vein endothelial cells (EC) stimulated with IL-1α, IL-1β, TNF-α or IL-1β+TNF-α. Inhibition required the presence of IVIG with the responding PMNs, was attributable to the F(ab)(2) portion and was unrelated to putative contaminants in IVIG.

Intravenous immunoglobulin G selectively inhibits IL-1α-induced neutrophil-endothelial cell adhesion.

Objectives: Intravenous immunoglobulin (IVIG) G at high doses has therapeutic benefits in a variety of autoimmune and inflammatory disorders. The mechanism by which IVIG modulates inflammation is incompletely understood. We tested the hypothesis that IVIG modulates inflammation by inhibiting interactions between neutrophils and vascular endothelium, required for leukocyte recruitment to inflamed tissues.

Intravenous immunoglobulin G-mediated inhibition of T-cell proliferation reflects an endogenous mechanism by which IgG modulates T-cell activation.

Commercial intravenous immunoglobulin G (IVIG) at high doses has therapeutic benefit in autoimmune and inflammatory diseases. It has been shown to inhibit T-cell function but the mechanisms are unclear. Inhibition could result from IVIG processing, donor pooling or intrinsic downregulatory activity of IgG.