Heat-induced aggregated human IgG modifies the adherence of human polymorphonuclear cells to cultured endothelium.

The adherence of human blood polymorphonuclear cells (PMNC) to cultured porcine aortic endothelium was enhanced by high concentrations of heat-stable IgG aggregates (HAGG) when sera was omitted from the culture media. With 20% human serum present in the media, HAGG induced a dose-related inhibition of PMNC adhesions with concentrations as low as 10 micrograms/ml producing a significant effect. This inhibitory action of HAGG, which was optimally expressed after 30 min of incubation, seemed to be directed at the PMNC rather than the endothelium. Heat-inactivation of the sera resulted in a marked decline of the inhibitory activity of HAGG. Aggregates of size 15-21 s were demonstrated to be most effective in inhibiting PMNC attachment and it is complexes of this size which are commonly found in the circulation of patients with chronic inflammatory diseases. Immune complex modification of PMNC adherence may control leucocyte extravasation during inflammation.