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Bcl-2 maintains B cell memory

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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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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