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Department of Immunology, Duke University Medical Center, Durham, NC 27710
The antiapoptotic protein Bcl-xL is induced in activated T lymphocytes upon costimulation through CD28, 4-1BB, and OX40. Bcl-xL is also highly enriched in memory T lymphocytes. Based on this body of evidence, it was thought that Bcl-xL plays an essential role in the generation of effector and memory T lymphocytes. We report that mice with a conditional deletion of Bcl-x in T lymphocytes develop a normal CD8+ T cell response to Listeria monocytogenes infection. Furthermore, Bcl-x conditional knockout mice exhibit normal T-dependent humoral immune responses. These results indicate that Bcl-x is dispensable for the generation of effector and memory T lymphocytes and suggest that costimulation of T lymphocytes promotes their survival through a Bcl-xL independent mechanism.
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