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Immune complexes inhibit apoptosis of chronic lymphocytic leukaemia B cells
Author(s) -
Gamberale Romina,
Geffner Jorge R.,
Trevani Analía,
Cherñavsky Alejandra,
Scolnik Mariano,
Arrosagaray Guillermo,
Sarmiento Marcela,
Giordano Mirta
Publication year - 1999
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.1999.01759.x
Subject(s) - apoptosis , chlorambucil , fludarabine , immune system , chronic lymphocytic leukemia , immunology , cancer research , biology , chemistry , microbiology and biotechnology , leukemia , chemotherapy , cyclophosphamide , biochemistry , genetics
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 IFNγ by non‐malignant cells upon activation with IC was responsible, to some extent, for IC effects as shown by the fact that neutralizing anti‐IFNγ 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.