IGM MONOCLONAL-ANTIBODIES RECOGNIZING FC-ALPHA-R BUT NOT FC-GAMMA-RIII TRIGGER A RESPIRATORY BURST IN NEUTROPHILS ALTHOUGH BOTH TRIGGER AN INCREASE IN INTRACELLULAR CALCIUM LEVELS AND DEGRANULATION

The role of IgG receptor, Fc gamma RIII, in the triggering of neutrophil functions has been controversial. Here we show that IgM monoclonal antibodies, Leu 11b and 1D3, recognizing Fc gamma RIII, bind to human neutrophils triggering an increase in intracellular calcium concentration and release of myeloperoxidase upon degranulation but do not trigger a respiratory burst detectable as lucigenin-enhanced chemiluminescence. Although many fewer molecules of IgM monoclonal antibody, MY43, recognizing Fc alpha R, bind to the same cells they trigger a much greater increase in intracellular calcium concentration, release of myeloperoxidase and a strong respiratory burst. Since the respiratory bursts triggered by IgG and IgA are equivalent, this demonstrates that Fc gamma RII is responsible for the IgG-mediated response. IgM monoclonal antibody MC2, recognizing the abundant neutrophil cell-surface carbohydrate CD15, also triggers a small rise in intracellular calcium but no respiratory burst.