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*
Laboratory of Immunology, Institute of Hematologic Research, National Academy of Medicine, and
Department of Microbiology, Buenos Aires University School of Medicine, Buenos Aires, Argentina
In the present study we examined whether immune complexes (IC) are
able to modulate human neutrophil apoptosis. We observed different
effects depending on the type of IC employed. Precipitating IC (pIC)
and Ab-coated erythrocytes (E-IgG) triggered a marked stimulation of
apoptosis, while heat-aggregated IgG and soluble IC, significantly
delayed spontaneous apoptosis. Blocking Abs directed to Fc
receptor
type II (FcRII), but not to FcRIII, markedly diminished the
acceleration of apoptosis triggered by either pIC or E-IgG, supporting
a critical role for FcRII in apoptosis stimulation. This phenomenon,
on the other hand, does not appear to involve IC phagocytosis or the
participation of CR3. Acceleration of neutrophil apoptosis triggered by
either pIC or E-IgG seems to require the activation of the respiratory
burst, as suggested by 1) the ability of catalase to prevent apoptosis
stimulation; 2) the effect of azide, an heme enzyme inhibitor, which
dramatically enhanced apoptosis induced by pIC or E-IgG; and 3) the
inability of pIC or E-IgG to accelerate apoptosis of neutrophils
isolated from CGD patients. It is well established that IC affect the
course of inflammation by inducing the release of inflammatory
cytokines, proteolytic enzymes, oxidative agents, and other toxic
molecules. Our results suggest that IC may also affect the course of
inflammation by virtue of their ability to modulate neutrophil
apoptosis.
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