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The Journal of Immunology, Vol 155, Issue 1 66-75, Copyright © 1995 by American Association of Immunologists
ARTICLES |
W Fang, JJ Rivard, JA Ganser, TW LeBien, KA Nath, DL Mueller and TW Behrens
Laboratory Medicine and Pathology, University of Minnesota, Minneapolis 55455, USA.
Developing lymphocytes undergo extensive cell death during selection of the immune repertoire. We investigated the influence of bcl-xL, a member of the bcl-2 family of apoptosis regulatory genes, on apoptosis in a model system for negative selection in the B lymphoid lineage. Overexpression of bcl-xL in WEHI 231 immature mouse B cells blocked apoptosis triggered by cross-linking of surface IgM. bcl-xL-transfected cells were also resistant to apoptosis following incubation in low serum medium or exposure to gamma-irradiation, the sphingomyelin ceramide, or compounds that increase intracellular levels of oxidants. Remarkably, the addition of antioxidants (catalase, N-acetylcysteine, or pyruvate) alone rescued the native WEHI 231 cells from apoptosis while having only minor effects on the viability of cells overexpressing bcl-xL. Anti-IgM cross-linking, ceramide, and gamma- irradiation treatments elevated intracellular peroxide production, which was prevented by treatment with antioxidants. Cells overexpressing bcl-xL had a similar rise in intracellular oxidants as control cells, indicating that bcl-xL modifies the cell's response to oxidants while having no detectable influence on the endogenous production of oxidants following apoptotic stimuli. These data implicate bcl-xL as a potent death repressor in B lymphocytes and support the hypothesis that bcl-xL regulates survival decisions within susceptible cells by functioning downstream of oxidant production.
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