The study investigates the effects of anti-neutrophil cytoplasmic autoantibodies (ANCA) on neutrophil function in vitro. ANCA, found in the serum of patients with pauci-immune necrotizing vasculitis and crescentic glomerulonephritis, are shown to induce oxidative bursts and degranulation in normal human neutrophils. Both cytoplasmic-pattern ANCA and myeloperoxidase (MPO)-specific ANCA activate neutrophils, leading to increased release of reactive oxygen species (ROS) and primary granule contents. These effects are enhanced by priming neutrophils with tumor necrosis factor (TNF). Flow cytometry confirms the presence of MPO on the surface of activated neutrophils, suggesting that ANCA interact with these antigens to initiate activation. The findings suggest that ANCA may play a pathogenic role in the development of vascular inflammation and glomerulonephritis by promoting the release of toxic oxygen radicals and harmful granule enzymes from cytokine-primed neutrophils.The study investigates the effects of anti-neutrophil cytoplasmic autoantibodies (ANCA) on neutrophil function in vitro. ANCA, found in the serum of patients with pauci-immune necrotizing vasculitis and crescentic glomerulonephritis, are shown to induce oxidative bursts and degranulation in normal human neutrophils. Both cytoplasmic-pattern ANCA and myeloperoxidase (MPO)-specific ANCA activate neutrophils, leading to increased release of reactive oxygen species (ROS) and primary granule contents. These effects are enhanced by priming neutrophils with tumor necrosis factor (TNF). Flow cytometry confirms the presence of MPO on the surface of activated neutrophils, suggesting that ANCA interact with these antigens to initiate activation. The findings suggest that ANCA may play a pathogenic role in the development of vascular inflammation and glomerulonephritis by promoting the release of toxic oxygen radicals and harmful granule enzymes from cytokine-primed neutrophils.