TFEB activation hallmarks antigenic experience of B lymphocytes and directs germinal center fate decisions.

ABSTRACT: Ligation of the B cell antigen receptor (BCR) initiates humoral immunity. However, BCR signaling without appropriate co-stimulation commits B cells to death rather than to differentiation into immune effector cells. How BCR activation depletes potentially autoreactive B cells while simultaneously primes for receiving rescue and differentiation signals from cognate T lymphocytes remains unknown. Here, we use a mass spectrometry-based proteomic approach to identify cytosolic/nuclear shuttling elements and uncover transcription factor EB (TFEB) as a central BCR-controlled rheostat that drives activation-induced apoptosis, and concurrently promotes the reception of co-stimulatory rescue signals by supporting B cell migration and antigen presentation. CD40 co-stimulation prevents TFEB-driven ce

SUBMITTER: Munchhalfen M 

PROVIDER: S-EPMC11322606 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature