In response to T cell-dependent Ag encounter, naive B cells develop into germinal center (GC) B cells, which can further differentiate into Ab-secreting plasma cells or memory B cells. GC B cells are short lived and are prone to caspase-mediated apoptosis. However, how apoptotic caspases regulate GC B cell fate has not been fully characterized. In this study, we show that mice with B cell-specific knockout of caspase-9 had decreases in GC B cells and Ab production after immunization. Caspase-9-deficient B cells displayed defects in caspase-dependent apoptosis but increases in necroptosis signaling. Additional deletion of Ripk3 restored GC B cells and Ab production in mice with B cell-specific knockout of caspase-9. Our results indicate that caspase-9 plays an important role in the maintenance of Ab responses by promoting apoptosis and inhibiting necroptosis in B cells.
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