Bifunctional lymphocyte regulation by human Fc gamma fragments and a synthetic peptide, p23, derived from the Fc region.

Fc fragments of human IgG1 and the synthetic peptide, p23, representing residues 335-357 in the CH3 domain of IgG1 were able to increase levels of secreted Ig in murine spleen cell cultures. B cell activation by Fc gamma fragments was macrophage- and T cell-dependent whereas activation by p23 was only T cell-dependent. Induction of Ig secretion by both stimulators was influenced by endogenous oxidative products of arachidonate, as evidenced by the augmentation of Ig levels in cell cultures treated with indomethacin (IM), a prostaglandin (PG) synthetase inhibitor. Both Fc gamma fragments and p23 were able to induce the release of PGE from splenic adherent macrophages and, in the former case, the release was inhibited by either IM or aspirin. Moreover, addition of either exogenous PGE1 or PGE2 reduced the levels of secreted Ig in Fc gamma fragment- or p23-stimulated cell cultures. These data suggest that B cell activation by Fc gamma fragments is influenced by the concomitant induction of suppressive PG.