Fig. 2.
Fig. 2. Study of the molecules implicated in the inhibitory effect. / BM cells from patients with B-CLL (1 × 106) were cultured in the presence and the absence of PMA-induced autologous B-CLL cells (1 × 106). Blocking mAb against a variety of adhesion molecules (A) and against CD95 and CD95L (B) were added to the latter coculture (10 μg/mL) as indicated. Values were expressed as percentages of control B-CLL BM IgG secretion (BM cells cultured alone). Results represent the mean ± SD of 8 experiments. Control IgG production in these experiments was 251 ± 64 ng/mL (mean ± SEM; n = 8).The continuous line indicates the mean inhibition of IgG production by PMA-induced B-CLL cells in these experiments. Significant reversal of the inhibitory effect was only observed for mAb anti-CD95 and anti-CD95L, as determined by the Student t test (P < .001 and P < .005, respectively).

Study of the molecules implicated in the inhibitory effect.

BM cells from patients with B-CLL (1 × 106) were cultured in the presence and the absence of PMA-induced autologous B-CLL cells (1 × 106). Blocking mAb against a variety of adhesion molecules (A) and against CD95 and CD95L (B) were added to the latter coculture (10 μg/mL) as indicated. Values were expressed as percentages of control B-CLL BM IgG secretion (BM cells cultured alone). Results represent the mean ± SD of 8 experiments. Control IgG production in these experiments was 251 ± 64 ng/mL (mean ± SEM; n = 8).The continuous line indicates the mean inhibition of IgG production by PMA-induced B-CLL cells in these experiments. Significant reversal of the inhibitory effect was only observed for mAb anti-CD95 and anti-CD95L, as determined by the Student t test (P < .001 and P < .005, respectively).

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