ACTIVATED PHENOTYPE IN NEUTROPHILS AND MONOCYTES FROM PATIENTS WITH PRIMARY PROLIFERATIVE POLYCYTHEMIA

Aim-To investigate whether monocytes and neutrophils from patients wit h primary proliferative polycythaemia (PPP) exhibit increased expressi on of markers of cell activation and, if so, whether they are associat ed with the phagocytic activity of these cells and concentrations of c irculating cytokines. Methods-Expression of CD11b, CD14, CD18, and CD6 4 on monocytes and neutrophils was assessed by flow cytometry. Phagocy tosis was analysed using immunoglobulin opsonised Escherichia coli. Se rum concentrations of granulocyte colony stimulating factor (G-CSF), g ranulocyte-macrophage CSF (GM-CSF) and macrophage CSF (IM-CSF) were de termined by bioassays, and interferon-gamma (IFN-gamma) by enzyme link ed immunosorbent assay (ELISA). Results-Patients with PPP (n = 18), wh en compared with normal subjects (n = 10), had increased percentages o f CD64+ monocytes (52% v 36%) and neutrophils (42% v 11%) and of CD14 neutrophils (36% v 18%). Monocytes from patients with PPP exhibited i ncreased expression of CD64 (47 v 26) and of CD11b (65 v 36). These ab normalities were not found in patients with secondary (n = 8) or appar ent (n = 13) polycythaemia. The percentage of neutrophils undergoing p hagocytosis was higher in patients with PPP (mean 64%; n = 6) than in normal subjects (mean 42%; n = 5). G-CSF, GM-CSF and IFN-gamma concent rations in patients' serum samples were comparable with normal; M-CSF was not detected in any of the samples. There was no correlation betwe en cytokine concentrations and the expression of CD11b, CD14, CD18, an d CD64 on patients' phagocytes. Conclusions-Increased expression of CD 11b and CD64 by monocytes, increased percentages of CD14+ and CD64+ ne utrophils and the high phagocytic activity of neutrophils suggests tha t these cells are activated in vivo in patients with PPP. The phenotyp ic changes of PPP phagocytes were not associated with increased concen trations of circulating cytokines and probably reflect intrinsic abnor malities within the neoplastic PPP clone.