Foxo3 Promotes Apoptosis of B Cell Receptor-Stimulated Immature B Cells, Thus Limiting the Window for Receptor Editing.

ABSTRACT: Central tolerance checkpoints are critical for the elimination of autoreactive B cells and the prevention of autoimmunity. When autoreactive B cells encounter their Ag at the immature B cell stage, BCR cross-linking induces receptor editing, followed by apoptosis if edited cells remain autoreactive. Although the transcription factor Foxo1 is known to promote receptor editing, the role of the related factor Foxo3 in central B cell tolerance is poorly understood. We find that BCR-stimulated immature B cells from Foxo3-deficient mice demonstrate reduced apoptosis compared with wild type cells. Despite this, Foxo3^-/- mice do not develop increased autoantibodies. This suggests that the increased survival of Foxo3^-/- immature B cells allows additional rounds of receptor edi

SUBMITTER: Ottens K 

PROVIDER: S-EPMC6057821 | biostudies-literature | 2018 Aug

REPOSITORIES: biostudies-literature