RESUMO
Effects of AML and normal mononuclear phagocyte conditioned media (CM) on the proliferation and differentiation of monoblastic human cell line U-937 have been studied. The normal mononuclear phagocyte CM inhibited proliferation and weakly stimulated differentiation of U-937 cells, whereas AML CM exerted no effect. Activation of both normal and AML macrophages with phorbol ether (TPA) was followed by enhancement of CM effect. TPA treatment corrected defects of secretory activity of AML mononuclear phagocytes. A possible role of different monokines in the regulation of proliferation and differentiation of leukaemic cells is discussed.
Assuntos
Leucemia Mieloide Aguda/imunologia , Macrófagos/metabolismo , Monócitos/metabolismo , Monocinas/farmacologia , Células da Medula Óssea , Diferenciação Celular/efeitos dos fármacos , Divisão Celular/efeitos dos fármacos , Humanos , Linfoma Difuso de Grandes Células B , Macrófagos/efeitos dos fármacos , Monócitos/efeitos dos fármacos , Monocinas/efeitos dos fármacos , Monocinas/metabolismo , Acetato de Tetradecanoilforbol/farmacologia , Células Tumorais CultivadasRESUMO
Data on long-term interferon-alpha (reaferon) therapy in 6 patients with CML (5 in chronic phase, 1 in acceleration phase) are presented. Clinicohematological remission was achieved in all the patients in a chronic phase irrespective of their group of risk. Cytogenetic improvement occurred only in one patient from a low-risk group. Reaferon had no effect in the patient in the acceleration phase. Tumor necrosis factor neither influenced viability of mononuclear bone marrow cells of patients before treatment nor suppressed proliferation. Dose independent reduction of cell viability was revealed in a patient in remission after reaferon therapy. There were no cases of apoptosis induction. Mechanisms of CML pathogenesis and interferon action in CML chronic phase are discussed.