Publication | Open Access
Differentiated HL60 promyelocytic leukaemia cells have a deficient myeloperoxidase/halide killing system.
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Citations
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References
1985
Year
Mixed-phenotype Acute LeukemiaImmunologyCell DeathRedox BiologyTumor BiologyOxidative StressMyeloid NeoplasiaInflammationHematological MalignancyInactive Mpo/peroxide/halideDeficient Myeloperoxidase/halideHematologyToxicologyOpsonized BacteriaCell SignalingGranulocyteReactive Oxygen SpeciePharmacologyCell BiologyPhagocyteMalignant Blood DisorderMedicineOxygen Radicals
Following induction of differentiation by incubation with 1.25% dimethylsulfoxide (DMSO), cells of the HL60 promyelocytic leukaemia cell line acquire certain characteristics of the mature polymorphonuclear leucocyte (PMN) including the ability to produce oxygen radicals and to phagocytose opsonized bacteria. However, these cells are unable to fix 125I during phagocytosis and are only able to kill phagocytosed microorganisms (C. albicans and S. aureus) to a small degree compared to mature PMN. Further, release of myeloperoxidase (MPO) from cytoplasmic granules occurs to approximately 20% of control levels after 6 days culture with DMSO, and drops to negligible levels by 7 days. These data suggest an immature or inactive MPO/peroxide/halide killing system. Insensitivity to the cyclooxygenase pathway inhibitor indomethacin suggests that there may also be a defect in this pathway.
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