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Blood, 1 November 2000, Vol. 96, No. 9, pp. 3168-3174
NEOPLASIA
Chronic lymphocytic leukemia B cells inhibit spontaneous Ig
production by autologous bone marrow cells: role of CD95-CD95L
interaction
Almudena Sampalo,
Gloria Navas,
Francisco Medina,
Carmen Segundo,
Carmen Cámara, and
José A. Brieva
From the Servicio de Inmunología, Hospital
Universitario Puerta del Mar, Cádiz, Spain.
A variable degree of humoral immunodeficiency is a common
feature in patients with B-cell chronic lymphocytic leukemia (B-CLL). The aim of this study was to explore the possibility that B-CLL cells
play a direct role in this phenomenon. To this end, patients' bone
marrow (BM) immunoglobulin (Ig)-secreting cells were cocultured with
autologous purified B-CLL cells. The results show that tumoral cells
inhibited the spontaneous IgG secretion by BM plasma cells, and this
effect increased after PMA-induction of B-CLL cells. This inhibitory
process was proportional to the number of B-CLL cells added and
depended on cellular contact. Adhesion molecules did not appear to be
involved in the cellular interaction, because the inclusion of blocking
antibody to a variety of these proteins did not reverse the inhibitory
phenomenon. However, the addition of monoclonal antibody that blocked
the function of either CD95 or CD95L clearly reversed B-CLL cell
inhibition on autologous BM plasma cells. These latter cells were shown
to express CD95, and B-CLL cells contained detectable quantities of
CD95L at the level of messenger RNA and protein. Annexin V-binding
experiments revealed increased apoptosis of BM Ig-secreting cells when
cocultured with autologous B-CLL cells. Finally, this inhibitory
phenomenon might be operative in vivo because (a) there was
a good correlation between the intensity of the inhibitory effect in
vitro and the serum IgG level exhibited by every patient and
(b) B-CLL cells also inhibited in vivo antigen-induced
IgG-tetanus toxoid-secreting cells obtained from normal immunized
subjects. Collectively, these data suggest that B-CLL cells inhibit
autologous CD95-bearing Ig-secreting cells by the interaction with
CD95L present on B-CLL cells and, hence, contribute to the state of
humoral immunodeficiency that occurs in these patients.
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