Loss of Fc receptor activity after culture of human monocytes on surface-bound immune complexes. Mediation by cyclic nucleotides.

Abstract

Human monocytes cultured on surface-bound immune complexes exhibited a loss of ability to form rosettes with IgG-sensitized sheep erythrocytes (EA). This loss was not a result of inhibition of Fc receptors by solubilized complexes nor of release of soluble factors by the cells. Loss of EA rosetting was not prevented by culture of monocytes at 4 degrees C, or by treatment with colchicine, cytochalasin B, or local anethetic agents. These results suggested that the loss was not secondary to capping or interiorization of Fc receptors. The results of other studies indicated that the Fc receptors were not damaged by lysosomal enzymes or oxygen radicals. Maintenance of EA rosetting ability of monocytes cultured on surface-bound immune complexes was seen after a 3-h preincubation of the cells in 100 mM 2-deoxy-D-glucose (2dG). A similar preincubation in ATP or in 8-bromoadenosine 3':5'-cyclic monophosphoric acid plus the phosphodiesterase inhibitor methyl isobutyl xanthine led to a partial loss of EA rosetting of cells on plain fibrin and to a partial reversal of the effects of 2dG seen with cells on complexes. We conclude that EA rosetting of monocytes cultured on surface-bound immune complexes is reduced by cyclic nucleotide-mediated effects on Fc receptor number or function.

Monocyte receptor function in patients with rheumatoid arthritis

“…Gormus et al suggested that on human lymphocytes, receptors for aggregated gamma globulin and EA are closely associated topographically on the cell membrane but are not identical (33). Ragsdale and Arend recently described the selective loss of Fc receptor activity for EA by normal monocytes plated on surface bound immune complexes (34). They did not find this loss when their monocytes plated on fibrin were incubated with low concentrations (2-10 pg/ml) of soluble HSA-anti HSA complexes.…”

Effects of soluble immune complexes on Fc receptor- and C3b receptor-mediated phagocytosis by macrophages.

“…These findings suggest that soluble immune complexes may also block Fc receptors, and results of the present experiments confirm that they can. Macrophage Fc receptor function can also be blocked by plating the cells on immobilized immune complexes (15,(28)(29)(30)(31); here, even the function of receptors on the nonbound surface of the macrophage is impaired. In each of these studies, the Fc receptor blockade was clearly mediated by immobilized and not by soluble complexes.…”

Reversible and irreversible loss of Fc receptor function of human monocytes as a consequence of interaction with immunoglobulin G.

“…7A). Because receptor loss is reversible, it is unlikely that receptor denaturation or internalization is important in the loss offunction as has been suggested by others (22 monomeric IgG (24) with a much slower rate of (issociation (26), we presume that the rapid loss of Fc receptor function following incubation ofmonocytes with concentrated solutions of purified aggregates results from the saturation of available receptors with IgGI aggregates. We attribute the return of function after trypsin treatment to the degradation of IgGI aggregates still bound to the receptors on the cell membrane.…”