Ectopic expression of BcI-2, but not BcI-xL rescues Ramos B cells from Fas-mediated apoptosis

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Abstract
The human Burkitt lymphoma Ramos B cell line can be induced to undergo apoptosis in response to a variety of different agents, including calcium ionophores, anti‐immunoglobulin (Ig) and macromolecular synthesis inhibitors. In addition, following up‐regulation of the Fas (CD95) surface receptor by CD40 ligation, these cells also become susceptible to apoptosis induction by Fas ligation. We have previously shown that protection from calcium ionophore‐ and macromolecular synthesis inhibitor‐induced apoptosis by CD40 ligation is associated with a rapid up‐regulation of BcI‐xL followed by a more moderate and delayed up‐regulation of BcI‐2. We show here that overexpression of BcI‐xL, like BcI‐2, protects Ramos cells from apoptosis induction in response to calcium ionophore, anti‐Ig and macromolecular synthesis inhibition. However, in contrast to BcI‐2, ectopic overexpression of BcI‐xL does not rescue from Fas‐mediated apoptosis. Thus, in Ramos B cells, the Fas apoptotic pathway exhibits differential sensitivity to inhibition by BcI‐2 family members. These findings also suggest that CD40 signaling provides a switch which renders the cells susceptible to Fas‐ligand mediated apoptosis through up‐regulation of Fas whilst affording protection from anti‐Ig‐induced apoptosis through up‐regulation of BcI‐xL.

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