We have investigated the role of neutrophil oxidants in the surface changes that result in recognition and uptake of neutrophils by macrophages. We have shown that H2O2 produced by stimulated neutrophils is essential for the surface expression of phosphatidylserine. This does not occur in neutrophils from mice with chronic granulomatous disease and may explain the formation of granuloma in this condition. We have also investigated the role of intracellular vitamin C on neutrophil apoptosis. Cells from vitamin C-deficient mice were found to be less likely to undergo both spontaneous and oxidant-induced apoptosis, with eventual necrosis being the most probable outcome.

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