Maintenance of Germinal Center B Cells by Caspase-9 through Promotion of Apoptosis and Inhibition of Necroptosis

J Immunol. 2020 Jul 1;205(1):113-120. doi: 10.4049/jimmunol.2000359. Epub 2020 May 20.


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • B-Lymphocytes
  • Caspase 9 / genetics
  • Germinal Center*
  • Mice
  • Mice, Knockout
  • Necroptosis*


  • Caspase 9