Immune complexes inhibit apoptosis of chronic lymphocytic leukaemia B cells.
In the present study we examined the effect of immune complexes (IC) on the survival of chronic lymphocytic leukaemia (B-CLL) B cells. Our results showed that either precipitating IC (pIC), Ab-coated erythrocytes (E-IgG) or heat-aggregated IgG (aIgG) significantly inhibited spontaneous apoptosis of B-CLL cells, as well as that induced by fludarabine, chlorambucil or dexamethasone. After depletion of T lymphocytes, monocytes and NK cells, incubation with IC was no longer able to delay B-CLL cells apoptosis, suggesting that prevention of apoptosis depends on IC interaction with accessory leucocytes. The release of IFNgamma by non-malignant cells upon activation with IC was responsible, to some extent, for IC effects as shown by the fact that neutralizing anti-IFNgamma MoAb partially prevented their ability to inhibit B-CLL cells apoptosis. The observation that treatment with IC resulted in increased expression of HLA-DR on B-CLL cells suggests that inhibition of apoptosis is associated with cellular activation.
Gamberale
R
R
Laboratory of Immunology, Institute of Haematologic Research, National Academy of Medicine, Buenos Aires, Argentina.
Geffner
J R
JR
Trevani
A
A
Cherñavsky
A
A
Scolnik
M
M
Arrosagaray
G
G
Sarmiento
M
M
Giordano
M
M
D000936:Antigen-Antibody Complex / Q000276:immunology*; D017209:Apoptosis / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology / Q000473:pathology*; D015536:Down-Regulation; D006684:HLA-DR Antigens / Q000378:metabolism; D006801:Humans; D007371:Interferon-gamma / Q000502:physiology; D015451:Leukemia, Lymphocytic, Chronic, B-Cell / Q000276:immunology* / Q000473:pathology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D017452:Receptors, IgG / Q000276:immunology
D000936:Antigen-Antibody Complex; D006684:HLA-DR Antigens; D019253:Proto-Oncogene Proteins c-bcl-2; D017452:Receptors, IgG; D007371:Interferon-gamma