Abstract

Rheumatoid sera and plasma inhibited the adherence of normal blood polymorphonuclear cells (PMNs) to cultured porcine endothelium. This inhibition of adhesion was not seen when PMNs were treated with the plasma or serum from normal subjects or patients with other inflammatory arthropathies. The abrogation of PMN adherence was directly related to the levels of circulating immune complexes and was not dependent upon the type of anti-inflammatory therapy that the patients were receiving nor on any of the recorded clinical parameters. A similar inhibition of adhesion was seen with heat induced aggregated human IgG (HAGG) provided that serum was present in the culture medium. In view of these results we propose that circulating immune complexes in RA may have a significant role in controlling the interaction of PMNs with vascular endothelium and in perpetuating the entry of these cells into the synovial fluid of the inflamed joints.