KINETICS OF INTERACTION OF IMMUNE-COMPLEXES WITH COMPLEMENT RECEPTORS ON HUMAN-BLOOD CELLS - MODIFICATION OF COMPLEXES DURING INTERACTION WITH RED-CELLS

  • 1 January 1982
    • journal article
    • research article
    • Vol. 48  (3) , 715-725
Abstract
Antigen-antibody complexes, composed of 125I-BSA [bovine serum albumin] and guinea-pig or rabbit antibody, were incubated at 37.degree. C with human blood cells suspended in autologous serum and kinetics of binding analyzed. When purified polymorphonuclear (PMN) or mononuclear cells (MNC) were studied, maximum binding was observed within 8 min, and immune complexes (IC) remained associated with cells even after 1 h. When cells were studied unseparated (in the same amount of serum), maximum binding was observed slightly earlier (within 4 min), but within 15 min most of the IC were found in the serum. Separation of cell types at the time of maximal binding and studies with cell preparations depleted of different elements revealed that binding was principally to red blood cells (RBC). IC recovered in the serum 16 min after addition to unseparated cells bound very slowly to purified PMN or MNC; binding after 30 min was 10-15% of that observed with fresh IC at 8 min. Ultracentrifugal analysis revealed that reduction in binding efficiency correlated with decrease in the size of IC. RBC isolated after binding and release of IC bound newly-formed IC with identical rapidity and capacity as fresh RBC, indicating that receptors were not altered by IC. Kinetics studies with serum in the absence of cells suggested that interaction with RBC accellerated the rate of change in binding properties of IC. Rates of binding and release were independent of antigen/antibody ratio but were slowed and binding to RBC sustained when diluted or hypocomplementemic (SLE [systemic lupus erythematosus]) serum was substituted for neat serum. Competition for IC by RBC is probably associated with loss of ability of IC to bind to other blood cell types and reduction in size of IC. Abnormalities of complement may lead to prolonged association of IC with RBC.