While there is much evidence for a key role of IgA in mucosal defence, its mode of action is incompletely understood. The finding of Fc receptors for IgA on various phagocytic cells has led to examination of the ability of IgA to mediate the protective functions of these cells. We studied the ability of human peripheral monocytes to secrete superoxide upon interaction with human IgA, IgG or IgM bound to a solid phase. Both secretory and serum IgA triggered the superoxide response, producing superoxide levels comparable to those induced by IgG, whereas IgM and mouse IgA were inactive. A combination of monomeric IgG and a monoclonal anti-IgG Fc receptor antibody inhibited superoxide secretion mediated through IgG but failed to block the IgA-triggered response, demonstrating that IgA was recognized through specific receptors. In addition IgA was capable of mediating phagocytosis when attached to erythrocytes.