Immune complexes and apoptosis in B-cell chronic lymphocytic leukemia.
The progressive accumulation of B-cell chronic lymphocytic leukemia (B-CLL) cells in vivo is attributed to resistance to apoptosis, although this can be modulated in vitro by a variety of cellular and humoral factors (cell-cell, cell-matrix interactions, cytokines). We have previously reported that IgG immune complexes (IC) delay B-CLL cell apoptosis through a paracrine mechanism, which depends on monocytes and NK cells. On the other hand, despite the fact that IC effectively bind to type II Fc gammaRs expressed on B-CLL cells, they are unable to deliver transmembrane signals. We speculate that this lack of responsiveness of resting B-CLL cells to IC could be overcome by activation. The analysis of this possibility would be relevant since the presence of circulating IC is a common feature in B-CLL patients.
Gamberale
Romina
R
Laboratorio de Immunologia, Instituto de Investigaciones Hematológicas, Academia de Medicina, Buenos Aires, Argentina.
Geffner
Jorge R
JR
Giordano
Mirta
M
D000818:Animals; D000936:Antigen-Antibody Complex / Q000276:immunology*; D017209:Apoptosis / Q000276:immunology*; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology; D015451:Leukemia, Lymphocytic, Chronic, B-Cell / Q000276:immunology* / Q000473:pathology; D017452:Receptors, IgG / Q000276:immunology
D000936:Antigen-Antibody Complex; D007074:Immunoglobulin G; D017452:Receptors, IgG