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 Ig[immunoglobulin]G-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.degree. C, or by treatment with colchicine, cytochalasin B or local anesthetic agents. The loss was apparently not secondary to capping or interiorization of Fc receptors. Results of other studies indicated that 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 partial loss of EA rosetting of cells on plain fibrin and to partial reversal of the effects of 2dG seen with cells on complexes. EA rosetting of monocytes cultured on surface-bound immune complexes is reduced by cyclic nucleotide-mediated effects on Fc receptor number or function.