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Bcl-2 maintains B cell memory

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Abstract

THE number of lymphocytes in an animal is remarkably constant despite antigen-driven proliferation and a high rate of B-cell lymphopoiesis. This reflects the relatively brief lifespan of many newly generated B cells and argues for a well-regulated death mechanism1–3. Even so, a secondary immune response can be generated years after a primary exposure to antigen4. Antigen that might restimulate B cells persists for extended periods on follicular dendritic cells in the light zone of germinal centres5–13. Antigen-binding B cells have also been found months after the end of obvious cell division14. The precise signal that enables certain B cells to emerge as long-term surviving memory cells14–17 is unknown. Bcl-2, an inner mitochondrial membrane protein18, blocks programmed cell death in B cells18–20. We report here that this proto-oncogene maintains immune responsiveness. Transgenic mice overproducing Bcl-2 have a long-term persistence of immunoglobulin-secreting cells and an extended lifetime for memory B cells.

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Authors and Affiliations

  1. Howard Hughes Medical Institute and the Departments of Medicine, Molecular Microbiology and Pathology, Washington University School of Medicine, Saint Louis, Missouri, 63110, USA

    Gabriel Nuñez, David Hockenbery, Timothy J. McDonnell, Craig M. Sorensen & Stanley J. Korsmeyer

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  1. Gabriel Nuñez
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  2. David Hockenbery
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  3. Timothy J. McDonnell
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  4. Craig M. Sorensen
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  5. Stanley J. Korsmeyer
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Nuñez, G., Hockenbery, D., McDonnell, T. et al. Bcl-2 maintains B cell memory. Nature 353, 71–73 (1991). https://doi.org/10.1038/353071a0

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