Evaluation of CR1 expression in neutrophils from chronic myeloid leukaemia: relationship between prognosis and cellular activity.
The expression of the complement receptor CR1 has been evaluated using an immunoalkaline phosphatase staining method on peripheral blood neutrophils and granulocyte precursors from 22 patients with chronic myeloid leukaemia (CML) and 15 healthy subjects. The immunocytochemical labelling pattern of CR1 was evaluated semiquantitatively on cell smears using three different anti-CR1 monoclonal antibodies. The scoring method showed that seven patients with CML had a marked reduction in CR1 expression which did not change with in vitro stimulation of neutrophils with phorbol-myristate-acetate (PMA) whereas control cells responded to PMA, increasing the receptor level two-fold. In addition, functional analysis of neutrophils with low CR1 expression from CML patients showed a very low cytolytic activity against K562 tumour target, suggesting a relationship between the cellular content of CR1 and neutrophil tumouricidal activity. The involvement of CR1 in neutrophil-mediated lysis is consistent with complete lack of tumour toxicity following receptor neutralization by anti-CR1 monoclonal antibodies. Interferon therapy improved CR1 expression and the cytolytic response of neutrophils in three out of five CML patients with a moderately low CR1 score. CML patients non-responding to interferon therapy and those with a very low CR1 score, independent of the clinical stage, progressed more rapidly into the advanced clinical stage and blastic crisis.
Lanza
F
F
Cattedra di Ematologia, Università di Ferrara, Italy.
Fagioli
F
F
Gavioli
R
R
Spisani
S
S
Malavasi
F
F
Castoldi
G L
GL
Traniello
S
S
D003179:Complement C3b / Q000378:metabolism*; D003602:Cytotoxicity, Immunologic; D006801:Humans; D007124:Immunoenzyme Techniques; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000276:immunology / Q000378:metabolism* / Q000628:therapy; D009504:Neutrophils / Q000276:immunology* / Q000378:metabolism / Q000502:physiology; D011379:Prognosis; D011951:Receptors, Complement / Q000032:analysis*; D017463:Receptors, Complement 3b; D011994:Recombinant Proteins
D000077190:Interferon alpha-2; D016898:Interferon-alpha; D011951:Receptors, Complement; D017463:Receptors, Complement 3b; D011994:Recombinant Proteins; D003179:Complement C3b