Immune complexes inhibit apoptosis of chronic lymphocytic leukaemia B cells.

GAMBERALE R, GEFFNER JR, TREVANI A, CHERÑAVSKY A, SCOLNIK M, ARROSAGARAY G, SARMIENTO M, GIORDANO M.

BRITISH JOURNAL OF HAEMATOLOGY

WILEY-BLACKWELL PUBLISHING, INC

Lugar: Londres; Año: 1999 vol. 197 p. 870 - 876

0007-1048

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.